Journal articles on the topic 'Burst potential'
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Brown, Colin H., Gareth Leng, Mike Ludwig, and Charles W. Bourque. "Endogenous Activation of Supraoptic Nucleus κ-Opioid Receptors Terminates Spontaneous Phasic Bursts in Rat Magnocellular Neurosecretory Cells." Journal of Neurophysiology 95, no. 5 (May 2006): 3235–44. http://dx.doi.org/10.1152/jn.00062.2006.
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Phasic activity in magnocellular neurosecretory vasopressin cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action potentials (spikes) are superimposed on plateau potentials that are generated by summation of depolarizing after-potentials (DAPs). Burst termination is believed to result from autocrine feedback inhibition of plateau potentials by the κ-opioid peptide, dynorphin, which is copackaged in vasopressin neurosecretory vesicles and exocytosed from vasopressin cell dendrites during phasic bursts. Here we tested this hypothesis, using intracellular recording in vitro to show that κ-opioid receptor antagonist administration enhanced plateau potential amplitude to increase postspike excitability during spontaneous phasic activity. The antagonist also increased postburst DAP amplitude in vitro, indicating that endogenous dynorphin probably reduces plateau potential amplitude by inhibiting the DAP mechanism. However, the κ-opioid receptor antagonist did not affect the slow depolarization that follows burst termination, suggesting that recovery from endogenous κ-opioid inhibition does not contribute to the slow depolarization. We also show, by extracellular single-unit recording, that that there is a strong random element in the timing of burst initiation and termination in vivo. Administration of a κ-opioid receptor antagonist eliminated the random element of burst termination but did not alter the timing of burst initiation. We conclude that dendritic dynorphin release terminates phasic bursts by reducing the amplitude of plateau potentials to reduce the probability of spike firing as bursts progress. By contrast, dendritic dynorphin release does not greatly influence the membrane potential between bursts and evidently does not influence the timing of burst initiation.
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Salmanpour, Aryan, Lyndon J. Brown, Craig D. Steinback, Charlotte W. Usselman, Ruma Goswami, and J. Kevin Shoemaker. "Relationship between size and latency of action potentials in human muscle sympathetic nerve activity." Journal of Neurophysiology 105, no. 6 (June 2011): 2830–42. http://dx.doi.org/10.1152/jn.00814.2010.
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We employed a novel action potential detection and classification technique to study the relationship between the recruitment of sympathetic action potentials (i.e., neurons) and the size of integrated sympathetic bursts in human muscle sympathetic nerve activity (MSNA). Multifiber postganglionic sympathetic nerve activity from the common fibular nerve was collected using microneurography in 10 healthy subjects at rest and during activation of sympathetic outflow using lower body negative pressure (LBNP). Burst occurrence increased with LBNP. Integrated burst strength (size) varied from 0.22 ± 0.07 V at rest to 0.28 ± 0.09 V during LBNP. Sympathetic burst size (i.e., peak height) was directly related to the number of action potentials within a sympathetic burst both at baseline ( r = 0.75 ± 0.13; P < 0.001) and LBNP ( r = 0.75 ± 0.12; P < 0.001). Also, the amplitude of detected action potentials within sympathetic bursts was directly related to the increased burst size at both baseline ( r = 0.59 ± 0.16; P < 0.001) and LBNP ( r = 0.61 ± 0.12; P < 0.001). In addition, the number of detected action potentials and the number of distinct action potential clusters within a given sympathetic burst were correlated at baseline ( r = 0.7 ± 0.1; P < 0.001) and during LBNP ( r = 0.74 ± 0.03; P < 0.001). Furthermore, action potential latency (i.e., an inverse index of neural conduction velocity) was decreased as a function of action potential size at baseline and LBNP. LBNP did not change the number of action potentials and unique clusters per sympathetic burst. It was concluded that there exists a hierarchical pattern of recruitment of additional faster conducting neurons of larger amplitude as the sympathetic bursts become stronger (i.e., larger amplitude bursts). This fundamental pattern was evident at rest and was not altered by the level of baroreceptor unloading applied in this study.
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Korn, S. J., J. L. Giacchino, N. L. Chamberlin, and R. Dingledine. "Epileptiform burst activity induced by potassium in the hippocampus and its regulation by GABA-mediated inhibition." Journal of Neurophysiology 57, no. 1 (January 1, 1987): 325–40. http://dx.doi.org/10.1152/jn.1987.57.1.325.
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Intracellular and extracellular recordings were made from pyramidal neurons in hippocampal slices in order to study spontaneous paroxysmal bursting induced by raising the extracellular potassium concentration from 3.5 to 8.5 mM. Extracellular recordings from all hippocampal subfields indicated that spontaneous bursts appeared to originate in region CA3c or CA3b as judged by burst onset. Burst intensity was also greatest in regions CA3b and CA3c and became progressively less toward region CA2. Intracellular recordings indicated that in 8.5 mM potassium, large spontaneous excitatory postsynaptic potentials (EPSPs), large burst afterhyperpolarizations, and rhythmic hyperpolarizing-depolarizing waves of membrane potential were invariably present in CA3c neurons. High potassium (8.5 mM) induced a positive shift (+9 mV) in the reversal potential of GABAergic inhibitory postsynaptic potentials (IPSPs) in CA3c neurons without changing input resistance or resting potential. This resulted in a drastic reduction in amplitude of the IPSP. Reduction of IPSP amplitude occurred before the onset of spontaneous bursting and was reversible upon return to normal potassium. A new technique to quantify the relative intensity of interictal-like burst discharges is described. Pentobarbital, diazepam, and GABA uptake inhibitors, which enhance GABA-mediated synaptic inhibition, reduced the intensity of potassium-induced bursts, whereas the GABA antagonist bicuculline increased burst intensity. Diphenylhydantoin and phenobarbital, anticonvulsants that have little effect on GABAergic inhibition, were without effect on spontaneous bursts. Burst frequency was reduced by bicuculline and 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol but was unaffected by other drugs. Reduction of slice temperature from 35 to 19 degrees C dramatically reduced burst intensity but did not markedly affect burst frequency. We hypothesize that high potassium induces a rise in intracellular chloride concentration, possibly by activating an inward KCl pump or by a passive Donnan effect, which results in a decreased IPSP amplitude. With inhibition suppressed, the large spontaneous EPSPs that appear in high potassium cause individual CA3c neurons to fire. A combination of synaptic and electrical interactions among CA3c cells then synchronizes discharges into interictal spike bursts.
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Robinson, H. P., M. Kawahara, Y. Jimbo, K. Torimitsu, Y. Kuroda, and A. Kawana. "Periodic synchronized bursting and intracellular calcium transients elicited by low magnesium in cultured cortical neurons." Journal of Neurophysiology 70, no. 4 (October 1, 1993): 1606–16. http://dx.doi.org/10.1152/jn.1993.70.4.1606.
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1. In Mg(2+)-free external solution, rat cortical neurons in cultured networks entered a stable firing mode, consisting of regular bursts of action potentials superimposed on long-lasting depolarizations. The average separation between bursts varied from culture to culture, but was usually between 5 and 20 s. The distribution of burst intervals followed a Gaussian or normal distribution, with a standard deviation of typically 10% of the average burst period. 2. A gradually depolarizing pacemaker potential was never observed between bursts, but the threshold for action potentials during the quiescent phase was > or = 10 mV above the resting potential. No progressive change in conductance or excitability was observed during the quiescent period. Intracellular stimulation of action potentials did not reproduce the long-lasting depolarization. 3. Switching from current clamp to voltage clamp at the resting potential revealed large postsynaptic currents, mainly excitatory but with a small inhibitory component, at the same phase and frequency as the spike bursts, showing that periodic synaptic input is responsible for the burst-depolarizations. The current could be eliminated by local application of 2-amino-5-phosphonovaleric acid (APV) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to the postsynaptic cell. In the presence of tetrodotoxin, irregular miniature excitatory postsynaptic currents were observed. 4. A fluorescent calcium indicator (fluo-3, 100 microM) was included in the whole-cell pipette solution, to allow simultaneous electrical and calcium measurements in the same cell. In current clamp, transient intracellular calcium increases were found, which were synchronized to the spike bursts. The Ca2+ rise lasted as long as the action potential burst, and was followed by an exponential decay considerably slower than that of the membrane potential. Calcium transients disappeared during voltage clamp at the resting potential, suggesting that calcium influx through voltage-dependent calcium channels greatly exceeds that through synaptic channels. 5. Multisite Ca2+ recording, after loading with fluo-3 acetoxymethyl (AM) ester, revealed that the onsets of burst-related calcium transients were synchronized in all active cells of each view-field, to within approximately 20 ms. Occasionally, secondary rhythms were observed in which only a subset of cells participated. The times to peak and the decay times of calcium transients varied among synchronized cells. 6. The pharmacology of the burst-related calcium transients was investigated by bath application of a variety of compounds.(ABSTRACT TRUNCATED AT 400 WORDS)
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Dicaprio, R. "Plateau potentials in motor neurons in the ventilatory system of the crab." Journal of Experimental Biology 200, no. 12 (January 1, 1997): 1725–36. http://dx.doi.org/10.1242/jeb.200.12.1725.
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The motor neurons in the crab ventilatory system have previously been considered to be passive output elements in that the generation of bursts of action potentials in these neurons during ventilation was thought to be due to cyclic inhibition and excitation from the interneurons in the ventilatory central pattern generator. This study demonstrates that the large-amplitude depolarization that underlies bursts of action potentials in ventilatory motor neurons is produced by a plateau potential. These motor neurons satisfy a number of the experimental tests that have been proposed for plateau potentials, such as triggering of the burst by a brief depolarization, termination of the burst by a hyperpolarizing input, and an all-or-none suppression of the depolarizing potential by the injection of hyperpolarizing current.
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Lu, S. M., W. Guido, and S. M. Sherman. "Effects of membrane voltage on receptive field properties of lateral geniculate neurons in the cat: contributions of the low-threshold Ca2+ conductance." Journal of Neurophysiology 68, no. 6 (December 1, 1992): 2185–98. http://dx.doi.org/10.1152/jn.1992.68.6.2185.
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1. Thalamic relay cells, including those of the lateral geniculate nucleus, display a low-threshold spike (LT spike), which is a large depolarization due to an increased Ca2+ conductance. Typically riding the crest of each LT spike is a burst of from two to seven action potentials, which we refer to as the LT burst. The LT spike is voltage dependent, because if the cell's resting membrane potential is more depolarized than roughly -60 mV, the LT spike is inactivated, but if more hyperpolarized, the spike is deinactivated and can be activated by a depolarization, such as from an afferent excitatory postsynaptic potential (EPSP). Thalamic relay cells thus display two response modes: a relay or tonic mode, when the cell is depolarized and LT spikes are inactivated, leading to tonic firing of action potentials; and a burst mode, when the cell is hyperpolarized and tends to respond with LT spikes and their associated bursts of action potentials. 2. We were interested in the contribution of the LT spike on the transmission of visually evoked signals through geniculate relay cells to visual cortex. We recorded intracellularly from geniculate cells in an anesthetized, paralyzed, in vivo cat preparation to study the effects of membrane voltage, and thus the presence or absence of LT spikes, on responses to drifting sine-wave gratings. We monitored the visually evoked responses of 14 geniculate neurons (6 X, 7 Y, and 1 unclassified) at different membrane potentials at which LT spikes were inactivated or deinactivated. 3. Changing membrane voltage during visual stimulation switched the response mode of every cell between the relay and burst modes. In the burst mode, LT spikes occurred in phase with the visual stimulus and not at rhythmic intervals uncorrelated to visual stimuli. To any given stimulus cycle, the cell responded usually with an LT burst or a tonic response, and rarely was more than one LT burst evoked by a stimulus cycle. Occasionally a single cycle evoked both an LT burst and tonic response, but always the LT burst occurred first. 4. The spatial tuning characteristics of the cells did not differ dramatically as a function of membrane potential, because the tuning of the LT bursts was quite similar to that of the tonic response component. Although we did not obtain complete temporal tuning properties, we did note that hyperpolarized cells responded reliably with LT bursts at several temporal frequencies. 5. A consistent difference was seen between the LT burst and tonic response components in terms of response linearity.(ABSTRACT TRUNCATED AT 400 WORDS)
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Wang, Yu-Feng, and Glenn I. Hatton. "Milk Ejection Burst-Like Electrical Activity Evoked in Supraoptic Oxytocin Neurons in Slices From Lactating Rats." Journal of Neurophysiology 91, no. 5 (May 2004): 2312–21. http://dx.doi.org/10.1152/jn.00697.2003.
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To examine the mechanisms underlying milk-ejection bursts of oxytocin (OT) neurons during suckling, both in vivo and in vitro studies were performed on supraoptic OT neurons from lactating rats. The bursts were first recorded extracellularly in anesthetized rats. Burst-related electrical parameters were essentially the same as previous reports except for a trend toward transient decreases in basal firing rates immediately preceding the burst. From putative OT neurons in slices with extracellular recordings, bursts that closely mimicked the in vivo bursts were elicited by phenylephrine, an α1-adrenoceptor agonist, in a low-Ca2+ medium. Moreover, in whole cell patch-clamp recordings, the in vitro bursts were recorded from immunocytochemically identified OT neurons. After a transient decrease in the basal firing rate, the in vitro bursts started with a sudden increase in the firing rate, quickly reaching a peak level, then gradually decaying, and ended with a postburst inhibition. A brief depolarization of the membrane potential and an increase in membrane conductance appeared after the onset of the burst. Spikes during a burst were characterized by a significant increase in the duration and decrease in the amplitude around the peak rate firing. These bursts were significantly different from short-lasting burst firing of vasopressin neurons in membrane potential changes, time to reach peak firing rate, spike amplitude and duration during peak rate firing. Our extensive analysis of these results suggests that the in vitro burst is a useful model for further study of mechanisms underlying milk-ejection bursts of OT neurons in vivo.
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Cohen, Dror, and Menahem Segal. "Network bursts in hippocampal microcultures are terminated by exhaustion of vesicle pools." Journal of Neurophysiology 106, no. 5 (November 2011): 2314–21. http://dx.doi.org/10.1152/jn.00969.2010.
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Synchronized network activity is an essential attribute of the brain. Yet the cellular mechanisms that determine the duration of network bursts are not fully understood. In the present study, synchronized network bursts were evoked by triggering an action potential in a single neuron in otherwise silent microcultures consisting of 4–30 hippocampal neurons. The evoked burst duration, ∼2 s, depended on the recovery time after a previous burst. While interburst intervals of 35 s enabled full-length bursts, they were shortened by half at 5-s intervals. This reduction in burst duration could not be attributed to postsynaptic parameters such as glutamate receptor desensitization, accumulating afterhyperpolarization, inhibitory tone, or sodium channel inactivation. Reducing extracellular Ca2+ concentration ([Ca2+]o) relieved the effect of short intervals on burst duration, while depletion of synaptic vesicles with α-latrotoxin gradually eliminated network bursts. Finally, a transient exposure to high [K+]o slowed down the recovery time following a burst discharge. We conclude that the limiting factor regulating burst duration is most likely the depletion of presynaptic resources.
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Golanov, E. V., and D. J. Reis. "Vasodilation evoked from medulla and cerebellum is coupled to bursts of cortical EEG activity in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 2 (February 1, 1995): R454—R467. http://dx.doi.org/10.1152/ajpregu.1995.268.2.r454.
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Cerebral blood flow (rCBF), measured by laser-Doppler flowmetry, spontaneously fluctuates at approximately 6 events/min in the anesthetized rat. These cerebrovascular waves (CWs) are preceded by simultaneous and synchronous bursts of electrocorticographic activity similar to burst-suppression/spindle-burst electroencephalogram patterns. Identical burst-CW complexes are evoked by single electrical pulses of specific sites in the cerebellar fastigial nucleus or rostral ventrolateral medulla. These consist, sequentially, of a constant initial triphasic (positive-negative-positive) potential reversing polarity in lamina V, variable afterbursts, and transient elevations of rCBF appearing approximately 1.2 s after burst onset. Evoked bursts are occluded by spontaneous bursts appearing < 50 s earlier. Procainization of the cortex reversibly blocks burst-CW complexes. Gradually increasing stimulus frequency proportionally increases the numbers of burst-CW complexes before rCBF rises. We conclude that spontaneous and evoked burst-CW complexes result from excitation of common neurons in lamina V. These intracortical “vasodilator” neurons are spontaneously excited by thalamocortical afferents generating burst-suppression electroencephalogram (EEG) patterns and excited reflexively by afferent signals from the fastigial nucleus or rostral ventrolateral medulla and couple intrinsic neuronal activity to local vascular mechanisms generating vasodilation.
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Hudetz, Anthony G., and Olga A. Imas. "Burst Activation of the Cerebral Cortex by Flash Stimuli during Isoflurane Anesthesia in Rats." Anesthesiology 107, no. 6 (December 1, 2007): 983–91. http://dx.doi.org/10.1097/01.anes.0000291471.80659.55.
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Background The degree of suppression of sensory functions during general anesthesia is controversial. Here, the authors investigated whether discrete flash stimuli induced cortical field potential responses at an isoflurane concentration producing burst suppression and compared the spatiotemporal properties and frequency spectra of flash-induced burst responses with those occurring spontaneously. Methods Rats were equipped with multiple epidural and intracortical electrodes to record cortical field potentials in the right hemisphere at several locations along the anterior-posterior axis. At isoflurane concentrations of 1.1, 1.4, and 1.8%, discrete light flashes were delivered to the left eye while cortical field potentials were continuously recorded. Results Isoflurane at 1.4-1.8% produced burst suppression. Each flash produced a visual evoked potential in the primary visual cortex followed by secondary bursting activity in more anterior regions. The average latency and duration of these bursts were 220 and 810 ms, respectively. The spontaneous and flash-induced bursts were similar in frequency, duration, and spatial distribution. They had maximum power in the frontal (primary motor) cortex with a dominant frequency of 10 Hz. Conclusions The results suggest that discrete flash stimuli activate the motor regions of the cerebral cortex during isoflurane anesthesia and that these activations are analogous with those that occur spontaneously during burst suppression. Electrocortical suppression of the cortex during anesthesia does not prevent its response to visual stimuli.
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Schwindt, Peter, and Wayne Crill. "Mechanisms Underlying Burst and Regular Spiking Evoked by Dendritic Depolarization in Layer 5 Cortical Pyramidal Neurons." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1341–54. http://dx.doi.org/10.1152/jn.1999.81.3.1341.
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Mechanisms underlying burst and regular spiking evoked by dendritic depolarization in layer 5 cortical pyramidal neurons. Apical dendrites of layer 5 pyramidal cells in a slice preparation of rat sensorimotor cortex were depolarized focally by long-lasting glutamate iontophoresis while recording intracellularly from their soma. In most cells the firing pattern evoked by the smallest dendritic depolarization that evoked spikes consisted of repetitive bursts of action potentials. During larger dendritic depolarizations initial burst firing was followed by regular spiking. As dendritic depolarization was increased further the duration (but not the firing rate) of the regular spiking increased, and the duration of burst firing decreased. Depolarization of the soma in most of the same cells evoked only regular spiking. When the dendrite was depolarized to a critical level below spike threshold, intrasomatic current pulses or excitatory postsynaptic potentials also triggered bursts instead of single spikes. The bursts were driven by a delayed depolarization (DD) that was triggered in an all-or-none manner along with the first Na+ spike of the burst. Somatic voltage-clamp experiments indicated that the action current underlying the DD was generated in the dendrite and was Ca2+ dependent. Thus the burst firing was caused by a Na+ spike-linked dendritic Ca2+spike, a mechanism that was available only when the dendrite was adequately depolarized. Larger dendritic depolarization that evoked late, constant-frequency regular spiking also evoked a long-lasting, Ca2+-dependent action potential (a “plateau”). The duration of the plateau but not its amplitude was increased by stronger dendritic depolarization. Burst-generating dendritic Ca2+spikes could not be elicited during this plateau. Thus plateau initiation was responsible for the termination of burst firing and the generation of the constant-frequency regular spiking. We conclude that somatic and dendritic depolarization can elicit quite different firing patterns in the same pyramidal neuron. The burst and regular spiking observed during dendritic depolarization are caused by two types of Ca2+-dependent dendritic action potentials. We discuss some functional implications of these observations.
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Basarsky, T. A., and A. S. French. "Intracellular measurements from a rapidly adapting sensory neuron." Journal of Neurophysiology 65, no. 1 (January 1, 1991): 49–56. http://dx.doi.org/10.1152/jn.1991.65.1.49.
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1. The femoral tactile spine of the cockroach contains a single sensory neuron with its cell body in the lumen of the spine. Step movements of the spine produce rapidly adapting bursts of action potentials that decay to 0 in 1 s. Previous work has shown that a large part of this adaptation occurs during action potential encoding. 2. Intracellular recordings from the tactile spine neuron were obtained by lowering a microelectrode through the spine lumen and penetrating the cell body. Injection of Lucifer yellow followed by fluorescence microscopy confirmed the morphology of the soma, with a diameter of 30 microns, and showed an axon of 9 microns leaving the spine and proceeding proximally along the femur. 3. Membrane-potential records were digitized and examined at high resolution during bursts of action potentials produced by depolarizing current pulses. No significant changes in action potential shape were detected during adaptation. However, the rate of depolarization between action potentials slowed dramatically during the burst. This slowing could be reduced and the burst substantially prolonged by chloramine-T (CT), an agent that reduces sodium channel inactivation in several preparations. 4. A 100 Hz sinusoidal current was superimposed on depolarizing current pulses to test for changes in membrane conductance during a burst of action potentials. No such changes were detected, indicating that rapid adaptation is not due to changes in membrane permeability.(ABSTRACT TRUNCATED AT 250 WORDS)
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Elson, R. C., K. T. Sillar, and B. M. Bush. "Identified proprioceptive afferents and motor rhythm entrainment in the crayfish walking system." Journal of Neurophysiology 67, no. 3 (March 1, 1992): 530–46. http://dx.doi.org/10.1152/jn.1992.67.3.530.
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1. In crayfish, Pacifastacus leniusculus, remotion of a walking leg stretches the thoraco-coxal (TC) muscle receptor organ (TCMRO), located at the leg's articulation with the thorax. In vitro, alternate stretch and release of the fourth leg's TCMRO entrained the centrally generated rhythmic motor output to that leg, with the remotor phase of the rhythm entraining to TCMRO stretch, the promoter phase to release. This coordination of motor bursts to afferent input corresponds to that of active, rhythmic movements in vivo. 2. Entrainment was rapid in onset (stable coordination resulting within the first or second stimulus cycle) and was relatively phase-constant (whatever the stimulus frequency, during 1:1 entrainment, remotor bursts began near the onset of stretch and promotor bursts began near the onset of release). Outside the range of 1:1 entrainment, 2:1, 1:2, and 1:3 coordination ratios (rhythm:stimulus) were encountered. Resetting by phasic stimulation of the TCMRO was complete and probabilistic: effective stimuli triggered rapid transitions between the two burst phases. 3. The TCMRO is innervated by two afferents, the nonspiking S and T fibers, which generate graded depolarizing receptor potentials in response to stretch. During proprioceptive entrainment, the more phasic T fiber depolarized and hyperpolarized more rapidly or in advance of the more tonic S fiber. These receptor potentials were modified differently in the two afferents by interaction with central synaptic inputs that were phase-locked to the entrained motor rhythm. 4. Injecting slow sinusoidal current into either afferent alone could entrain motor rhythms: promoter phase bursts were entrained to depolarization of the S fiber or hyperpolarization of the T fiber, whereas the converse response was obtained for remotor phase bursts. 5. During proprioceptive entrainment, tonic hyperpolarization of the S fiber weakened entrained promotor bursts and allowed remotor burst durations to increase. Hyperpolarizing the T fiber weakened entrained remotor bursts and allowed promotor bursts to occur during stretch. These results suggest that the staggered receptor potentials of the two afferents alternately excite opposite burst phases of the rhythm during proprioceptive entrainment. 6. Injecting brief current pulses into either afferent perturbed the timing of entrained bursts in opposite ways, suggesting that, during proprioceptive entrainment, the membrane potential trajectories of the two afferents have reciprocal triggering effects on burst transitions. 7. We infer that entrainment results from 1) complete resetting of burst transitions in a two-phase central oscillator, 2) opposing feedback pathways mediated by a phasic and a tonic afferent, 3) temporally staggered afferent receptor potentials, and 4) the ability of afferent receptor potentials to trigger burst transitions.
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Hilmarsson, G. H., L. G. Spitler, E. F. Keane, T. M. Athanasiadis, E. Barr, M. Cruces, X. Deng, et al. "Observing superluminous supernovae and long gamma-ray bursts as potential birthplaces of repeating fast radio bursts." Monthly Notices of the Royal Astronomical Society 493, no. 4 (March 17, 2020): 5170–80. http://dx.doi.org/10.1093/mnras/staa701.
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ABSTRACT Superluminous supernovae (SLSNe) and long gamma-ray bursts (LGRBs) have been proposed as progenitors of repeating fast radio bursts (FRBs). In this scenario, bursts originate from the interaction between a young magnetar and its surrounding supernova remnant (SNR). Such a model could explain the repeating, apparently non-Poissonian nature of FRB121102, which appears to display quiescent and active phases. This bursting behaviour is better explained with a Weibull distribution, which includes parametrization for clustering. We observed 10 SLSNe/LGRBs for 63 h, looking for repeating FRBs with the Effelsberg 100-m radio telescope, but have not detected any bursts. We scale the burst rate of FRB121102 to an FRB121102-like source inhabiting each of our observed targets, and compare this rate to our upper burst rate limit on a source by source basis. By adopting a fiducial beaming fraction of 0.6, we obtain 99.99 per cent and 83.4 per cent probabilities that at least one, and at least half of our observed sources are beamed towards us, respectively. One of our SLSN targets, PTF10hgi, is coincident with a persistent radio source, making it a possible analogue to FRB121102. We performed further observations on this source using the Effelsberg 100-m and Parkes 64-m radio telescopes. Assuming that PTF10hgi contains an FRB121102-like source, the probabilities of not detecting any bursts from a Weibull distribution during our observations are 14 per cent and 16 per cent for Effelsberg and Parkes, respectively. We conclude by showing that a survey of many short observations increases burst detection probability for a source with Weibull distributed bursting activity.
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Bush, Paul C., and Rodney J. Douglas. "Synchronization of Bursting Action Potential Discharge in a Model Network of Neocortical Neurons." Neural Computation 3, no. 1 (February 1991): 19–30. http://dx.doi.org/10.1162/neco.1991.3.1.19.
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We have used the morphology derived from single horseradish peroxidase-labeled neurons, known membrane conductance properties and microanatomy to construct a model neocortical network that exhibits synchronized bursting. The network was composed of interconnected pyramidal (excitatory) neurons with different intrinsic burst frequencies, and smooth (inhibitory) neurons that provided global feedback inhibition to all of the pyramids. When the network was activated by geniculocortical afferents the burst discharges of the pyramids quickly became synchronized with zero average phase-shift. The synchronization was strongly dependent on global feedback inhibition, which acted to group the coactivated bursts generated by intracortical reexcitation. Our results suggest that the synchronized bursting observed between cortical neurons responding to coherent visual stimuli is a simple consequence of the principles of intracortical connectivity.
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Reinagel, Pamela, Dwayne Godwin, S. Murray Sherman, and Christof Koch. "Encoding of Visual Information by LGN Bursts." Journal of Neurophysiology 81, no. 5 (May 1, 1999): 2558–69. http://dx.doi.org/10.1152/jn.1999.81.5.2558.
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Encoding of visual information by LGN bursts. Thalamic relay cells respond to visual stimuli either in burst mode, as a result of activation of a low-threshold Ca2+ conductance, or in tonic mode, when this conductance is inactive. We investigated the role of these two response modes for the encoding of the time course of dynamic visual stimuli, based on extracellular recordings of 35 relay cells from the lateral geniculate nucleus of anesthetized cats. We presented a spatially optimized visual stimulus whose contrast fluctuated randomly in time with frequencies of up to 32 Hz. We estimated the visual information in the neural responses using a linear stimulus reconstruction method. Both burst and tonic spikes carried information about stimulus contrast, exceeding one bit per action potential for the highest variance stimuli. The “meaning” of an action potential, i.e., the optimal estimate of the stimulus at times preceding a spike, was similar for burst and tonic spikes. In within-trial comparisons, tonic spikes carried about twice as much information per action potential as bursts, but bursts as unitary events encoded about three times more information per event than tonic spikes. The coding efficiency of a neuron for a particular stimulus is defined as the fraction of the neural coding capacity that carries stimulus information. Based on a lower bound estimate of coding efficiency, bursts had ∼1.5-fold higher efficiency than tonic spikes, or 3-fold if bursts were considered unitary events. Our main conclusion is that both bursts and tonic spikes encode stimulus information efficiently, which rules out the hypothesis that bursts are nonvisual responses.
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Merlin, L. R., G. W. Taylor, and R. K. Wong. "Role of metabotropic glutamate receptor subtypes in the patterning of epileptiform activities in vitro." Journal of Neurophysiology 74, no. 2 (August 1, 1995): 896–900. http://dx.doi.org/10.1152/jn.1995.74.2.896.
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1. Epileptiform activities were elicited from the in vitro guinea pig hippocampus by the addition of picrotoxin. Modification of the picrotoxin-induced activities by agents active at metabotropic glutamate receptors (mGluRs) was examined using intracellular and extracellular recordings. 2. Picrotoxin typically elicited synchronized discharges (epileptiform bursts) in CA3 neurons. These spontaneously occurred at regular intervals. In the presence of (+)-alpha-methyl-4-carboxyphenylglycine (MCPG; 700–1,000 microM), an antagonist at multiple mGluR subtypes, the frequency of spontaneous epileptiform bursts decreased. In contrast, when the mGluR agonists (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD; 5 microM) or (2S,3S,4S)-alpha-(carboxycyclopropyl)-glycine (L-CCG-I; 10 microM) were added to the incubating medium, the frequency of epileptiform bursts increased. No consistent change in membrane potential, burst duration, nor burst afterhyperpolarization was associated with the changes in burst frequency. 3. When spontaneous burst frequency was reduced in MCPG, stimulation at a higher frequency entrained bursts without failure. Bursts evoked in MCPG were similar in waveform and amplitude to those evoked in the control state. 4. (S)-4-carboxyphenylglycine (S-4CPG) and (R,S)-4-carboxy-3-hydroxyphenylglycine (RS-4C3HPG) are antagonists at mGluR subtypes 1 and 5 but agonists at mGluRs 2 and 3. Addition of either of these agents increased the frequency of epileptiform bursts. 5. These results suggest that sufficient glutamate is released during epileptiform activities to activate mGluRs. The overall effect is to increase the frequency of synchronized discharges. This modulatory action on burst frequency is probably mediated via the mGluR 2 and 3 receptor subclass.
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Misiunas, D., M. Lambert, A. Simpson, and G. Olsson. "Burst detection and location in water distribution networks." Water Supply 5, no. 3-4 (November 1, 2005): 71–80. http://dx.doi.org/10.2166/ws.2005.0085.
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An algorithm for the detection and location of sudden bursts in water distribution networks combining both continuous monitoring of pressure and hydraulic transient computation is presented. The approach is designed for medium and large bursts that are the result of the sudden rupture of the pipe wall or other physical element in the network and are accompanied by the transient pressure wave that propagates throughout the network. The burst-induced transient wave arrival times and magnitudes measured at two or more points are used to find the location of a burst. The wave arrival times and magnitudes are detected using the modified cumulative sum (CUSUM) change detection test. Results of validation on a real network show the potential of the proposed burst detection and location technique to be used in water distribution systems.
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Bracci, E., L. Ballerini, and A. Nistri. "Spontaneous rhythmic bursts induced by pharmacological block of inhibition in lumbar motoneurons of the neonatal rat spinal cord." Journal of Neurophysiology 75, no. 2 (February 1, 1996): 640–47. http://dx.doi.org/10.1152/jn.1996.75.2.640.
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1. The effects of blocking gamma-aminobutyric acid- and glycine-mediated synaptic transmission by bicuculline and strychnine on the neonatal rat isolated spinal cord were investigated by intracellular recording from motoneurons with the use of current-clamp and voltage-clamp techniques and by extracellular recording from homologous ventral roots of the L5 segment. 2. Bicuculline per se evoked irregular bursts of motoneuron membrane potential, often comprising individual events fused together. Strychnine alone did not elicit spontaneous bursting in the large majority of preparations. Simultaneous application of bicuculline and strychnine consistently induced regular rhythmic bursts (frequency approximately 2 per min, duration approximately 7 s), comprising a rapid depolarization followed by large-amplitude oscillations. 3. Burst frequency, duration, and intraburst oscillation time course were independent of motoneuron membrane potential. Burst and oscillation amplitude decreased with membrane depolarization and, under voltage-clamp conditions, inverted polarity near 0 mV. 4. The regular bursts produced by bicuculline and strychnine were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione, tetrodotoxin, or Cd2+. 5. N-methyl-D-aspartate antagonists [R-5-aminophosphonovalerate or 3-((RS)-2-carboxypiperazine-4-yl)-propyl-1-phosphonate (CPP)] reversibly blocked or slowed down bursting induced by bicuculline and strychnine. Addition of cyclothiazide to the bicuculline and strychnine solution increased bursting frequency while preserving the regular burst structure; under these conditions bursts became insensitive to CPP. 6. In the presence of bicuculline and strychnine, 5-hydroxytryptamine (5-HT) increased burst frequency and decreased burst duration in a dose-dependent fashion. 7. In the presence of bicuculline and strychnine, L5 ventral roots developed synchronous rhythmic activity with a time course similar to that recorded from individual motoneurons. The rhythmic activity was accelerated by 5-HT on both roots, in accordance with observations on single motoneurons. 8. Rhythmic bursts thus appear to result from large, synchronous synaptic events generated by a network modulated by 5-HT and highly sensitive to variations in efficacy of glutamatergic synaptic transmission. These results show that in the rat spinal cord highly patterned motor output can occur despite block of inhibition.
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Kumar, K., S. Kumar Sinha, A. Kumar Bharti, and A. Barman. "Comparison of vestibular evoked myogenic potentials elicited by click and short duration tone burst stimuli." Journal of Laryngology & Otology 125, no. 4 (October 19, 2010): 343–47. http://dx.doi.org/10.1017/s0022215110001908.
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AbstractIntroduction:Vestibular evoked myogenic potentials are short latency electrical impulses that are produced in response to higher level acoustic stimuli. They are used clinically to diagnose sacculocollic pathway dysfunction.Aim:This study aimed to compare the vestibular evoked myogenic potential responses elicited by click stimuli and short duration tone burst stimuli, in normal hearing individuals.Method:Seventeen subjects participated. In all subjects, we assessed vestibular evoked myogenic potentials elicited by click and short duration tone burst stimuli.Results and conclusion:The latency of the vestibular evoked myogenic potential responses (i.e. the p13 and n23 peaks) was longer for tone burst stimuli compared with click stimuli. The amplitude of the p13–n23 waveform was greater for tone burst stimuli than click stimuli. Thus, the click stimulus may be preferable for clinical assessment and identification of abnormalities as this stimulus has less variability, while a low frequency tone burst stimulus may be preferable when assessing the presence or absence of vestibular evoked myogenic potential responses.
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Morgado-Valle, Consuelo, Juan Fernandez-Ruiz, Leonor Lopez-Meraz, and Luis Beltran-Parrazal. "Substitution of extracellular Ca2+ by Sr2+ prolongs inspiratory burst in pre-Bötzinger complex inspiratory neurons." Journal of Neurophysiology 113, no. 4 (February 15, 2015): 1175–83. http://dx.doi.org/10.1152/jn.00705.2014.
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The pre-Bötzinger complex (preBötC) underlies inspiratory rhythm generation. As a result of network interactions, preBötC neurons burst synchronously to produce rhythmic premotor inspiratory activity. Each inspiratory burst consists of action potentials (APs) on top of a 10- to 20-mV synchronous depolarization lasting 0.3–0.8 s known as inspiratory drive potential. The mechanisms underlying the initiation and termination of the inspiratory burst are unclear, and the role of Ca2+ is a matter of intense debate. To investigate the role of extracellular Ca2+ in inspiratory burst initiation and termination, we substituted extracellular Ca2+ with Sr2+. We found for the first time an ionic manipulation that significantly interferes with burst termination. In a rhythmically active slice, we current-clamped preBötC neurons ( Vm ≅ −60 mV) while recording integrated hypoglossal nerve (∫XIIn) activity as motor output. Substitution of extracellular Ca2+ with either 1.5 or 2.5 mM Sr2+ significantly prolonged the duration of inspiratory bursts from 653.4 ± 30.7 ms in control conditions to 981.6 ± 78.5 ms in 1.5 mM Sr2+ and 2,048.2 ± 448.5 ms in 2.5 mM Sr2+, with a concomitant increase in decay time and area. Substitution of extracellular Ca2+ by Sr2+ is a well-established method to desynchronize neurotransmitter release. Our findings suggest that the increase in inspiratory burst duration is determined by a presynaptic mechanism involving desynchronization of glutamate release within the network.
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Igin, I. M., A. V. Minin, E. V. Kuzmin, M. Yu Bamborin, S. L. Speshilov, and Iu V. Trofimova. "Potential Manifestations of Rock Bursts During URF Construction and Methods of their Prevention." Radioactive Waste 21, no. 4 (2022): 70–77. http://dx.doi.org/10.25283/2587-9707-2022-4-70-77.
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At great depths, the Yeniseiskiy section of the Nizhnekanskiy rock mass selected for the construction of an underground research facility (URF) may involve some areas of firm rocks with high internal stresses that may cause spontaneous rock bursts. The paper provides a qualitative description of the mechanism standing behind the rock burst process, the necessary and sufficient conditions for its occurrence and the conditions for its extinction. It considers some engineering methods dealing with rock bursts which may be applied given special requirements set out for the URF construction.
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Klassen, Stephen A., M. Erin Moir, Jacqueline K. Limberg, Sarah E. Baker, Wayne T. Nicholson, Timothy B. Curry, Michael J. Joyner, and J. Kevin Shoemaker. "Asynchronous action potential discharge in human muscle sympathetic nerve activity." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 4 (October 1, 2019): H754—H764. http://dx.doi.org/10.1152/ajpheart.00258.2019.
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What strategies are employed by the sympathetic system to communicate with the circulation? Muscle sympathetic nerve activity (MSNA) occurs in bursts of synchronous action potential (AP) discharge, yet whether between-burst asynchronous AP firing exists remains unknown. Using multiunit microneurography and a continuous wavelet transform to isolate APs, we studied AP synchronicity within human MSNA. Asynchronous APs were defined as those which occurred between bursts. Experiment 1 quantified AP synchronicity in eight individuals at baseline (BSL), −10 mmHg lower body negative pressure (LBNP), −40 mmHg LBNP, and end-expiratory apnea (APN). At BSL, 33 ± 12% of total AP activity was asynchronous. Asynchronous discharge was unchanged from BSL (67 ± 37 AP/min) to −10 mmHg LBNP (69 ± 33 AP/min), −40 mmHg LBNP (83 ± 68 AP/min), or APN (62 ± 39 AP/min). Across all conditions, asynchronous AP probability and frequency decreased with increasing AP size. Experiment 2 examined the impact of the ganglia on AP synchronicity by using nicotinic blockade (trimethaphan). The largest asynchronous APs were derecruited from BSL (11 ± 4 asynchronous AP clusters) to the last minute of the trimethaphan infusion with visible bursts (7 ± 2 asynchronous AP clusters). However, the 6 ± 2 smallest asynchronous AP clusters could not be blocked by trimethaphan and persisted to fire 100 ± 0% asynchronously without forming bursts. Nonnicotinic ganglionic mechanisms affect some, but not all, asynchronous activity. The fundamental behavior of human MSNA contains between-burst asynchronous AP discharge, which accounts for a considerable amount of BSL activity. NEW & NOTEWORTHY Historically, sympathetic nerve activity destined for the blood vessels supplying skeletal muscle (MSNA) has been characterized by spontaneous bursts formed by synchronous action potential (AP) discharge. However, this study found a considerable amount (~30% during baseline) of sympathetic AP discharge to fire asynchronously between bursts of human MSNA. Trimethaphan infusion revealed that nonnicotinic ganglionic mechanisms contribute to some, but not all, asynchronous discharge. Asynchronous sympathetic AP discharge represents a fundamental behavior of MSNA.
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Doiron, Brent, André Longtin, Ray W. Turner, and Leonard Maler. "Model of Gamma Frequency Burst Discharge Generated by Conditional Backpropagation." Journal of Neurophysiology 86, no. 4 (October 1, 2001): 1523–45. http://dx.doi.org/10.1152/jn.2001.86.4.1523.
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Pyramidal cells of the electrosensory lateral line lobe (ELL) of the weakly electric fish Apteronotus leptorhynchus have been shown to produce oscillatory burst discharge in the γ-frequency range (20–80 Hz) in response to constant depolarizing stimuli. Previous in vitro studies have shown that these bursts arise through a recurring spike backpropagation from soma to apical dendrites that is conditional on the frequency of action potential discharge (“conditional backpropagation”). Spike bursts are characterized by a progressive decrease in inter-spike intervals (ISIs), and an increase of dendritic spike duration and the amplitude of a somatic depolarizing afterpotential (DAP). The bursts are terminated when a high-frequency somatic spike doublet exceeds the dendritic spike refractory period, preventing spike backpropagation. We present a detailed multi-compartmental model of an ELL basilar pyramidal cell to simulate somatic and dendritic spike discharge and test the conditions necessary to produce a burst output. The model ionic channels are described by modified Hodgkin-Huxley equations and distributed over both soma and dendrites under the constraint of available immunocytochemical and electrophysiological data. The currents modeled are somatic and dendritic sodium and potassium involved in action potential generation, somatic and proximal apical dendritic persistent sodium, and KV3.3 and fast transient A-like potassium channels distributed over the entire model cell. The core model produces realistic somatic and dendritic spikes, differential spike refractory periods, and a somatic DAP. However, the core model does not produce oscillatory spike bursts with constant depolarizing stimuli. We find that a cumulative inactivation of potassium channels underlying dendritic spike repolarization is a necessary condition for the model to produce a sustained γ-frequency burst pattern matching experimental results. This cumulative inactivation accounts for a frequency-dependent broadening of dendritic spikes and results in a conditional failure of backpropagation when the intraburst ISI exceeds dendritic spike refractory period, terminating the burst. These findings implicate ion channels involved in repolarizing dendritic spikes as being central to the process of conditional backpropagation and oscillatory burst discharge in this principal sensory output neuron of the ELL.
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Schmidt, Sydney M. L., Charlotte W. Usselman, Eric Martinek, Michael K. Stickland, Colleen G. Julian, Radha Chari, Rshmi Khurana, Sandra T. Davidge, Margie H. Davenport, and Craig D. Steinback. "Activity of muscle sympathetic neurons during normotensive pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 2 (February 1, 2018): R153—R160. http://dx.doi.org/10.1152/ajpregu.00121.2016.
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In pathological populations, elevated sympathetic activity is associated with increased activity of individual sympathetic neurons. We used custom action potential detection software to analyze multiunit sympathetic activity in 18 normotensive pregnant women (third trimester; 33 ± 5 wk) and 19 nonpregnant women at rest and a subset (10 and 13, respectively) during a cold pressor challenge. Although the number of action potentials per burst and number of active amplitude-based “clusters” were not different between groups, the total number of sympathetic action potentials per minute was higher in pregnant women at rest. Individual clusters were active predominately once per burst, suggesting they represent single neurons. Action potentials occurred in closer succession in normotensive pregnant (interspike interval 36 ± 10 ms) versus nonpregnant women (50 ± 27 ms; P < 0.001) at rest. Pregnant women had a lower total peripheral resistance (11.7 ± 3.0 mmHg·l−1·min) than nonpregnant women (15.1 ± 2.7 mmHg·l−1·min; P < 0.001), indicating a blunted neurovascular transduction. The cold pressor reduced the number of action potentials per burst in both groups due to shortening of the R-R interval in conjunction with increased burst frequency; total neural firing per minute was unchanged. Thus elevated sympathetic activity during normotensive pregnancy is specific to increased incidence of multiunit bursts. This is likely due to decreased central gating of burst output as opposed to generalized increases in central drive. These data also reinforce the concept that pregnancy appears to be the only healthy state of chronic sympathetic hyperactivity of which we are aware.
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Vorobyov, Eduard I., Vardan G. Elbakyan, Michihiro Takami, and Hauyu B. Liu. "Effect of luminosity outbursts on protoplanetary disk dynamics." Astronomy & Astrophysics 643 (October 27, 2020): A13. http://dx.doi.org/10.1051/0004-6361/202038122.
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Aims. The response of a protoplanetary disk to luminosity bursts of various durations is studied with the purpose to determine the effect of the bursts on the strength and sustainability of gravitational instability in the disk. A special emphasis is paid to the spatial distribution of gas and grown dust (from 1 mm to a few centimetres) during and after the burst. Methods. Numerical hydrodynamics simulations were employed to study the dynamics of gas and dust in the thin-disk limit. Dust-to-gas friction, including back reaction and dust growth, were also considered. Bursts of various durations (from 100 yr to 500 yr) were initiated in accordance with a thermally ignited magnetorotational instability. Luminosity curves for constant- and declining-magnitude bursts were adopted to represent two typical limiting cases for FU Orionis-type eruptions. Results. The short-term effect of the burst is to reduce the strength of gravitational instability by heating and expanding the disk. The longest bursts with durations comparable to the revolution period of the spiral can completely dissolve the original two-armed spiral pattern in the gas disk by the end of the burst, while the shortest bursts only weaken the spiral pattern. The reaction of grown dust to the burst is somewhat different. The spiral-like initial distribution with deep cavities in the inter-armed regions transforms into a ring-like distribution with deep gaps. This transformation is mostly expressed for the longest-duration bursts. The long-term effect of the burst depends on the initial disk conditions at the onset of the burst. In some cases, vigorous disk fragmentation sets in several thousands of years after the burst, which was absent in the model without the burst. Several clumps with masses in the giant-planet mass range form in the outer disk regions. After the disk fragmentation phase, the spatial distribution of grown dust is characterized by multiple sharp rings located from tens to hundreds of astronomical units. The arrangement and sharpness of the rings depends on the strength of dust turbulent diffusion. The wide-orbit rings are likely formed as the result of dust-rich clump dispersal in the preceding gravitationally unstable phase. Conclusions. Luminosity bursts similar in magnitude to FU Orionis-type eruptions can have a profound effect on the dynamics of gas and dust in protoplanetary disks if the burst duration is comparable to, or longer than, the dynamical timescales. In this context, the spatial morphology of the gas-dust disk of V883 Ori, a FU Orionis-like object that is thought to be in the outburst phase for more than a century with an unknown onset date, may be used as test case for the burst models considered in this work. The potential relation of the obtained ring structures to a variety of gaps and rings observed in T Tauri disks remains to be established.
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Platts, E., M. Caleb, B. W. Stappers, R. A. Main, A. Weltman, J. P. Shock, M. Kramer, et al. "An analysis of the time-frequency structure of several bursts from FRB 121102 detected with MeerKAT." Monthly Notices of the Royal Astronomical Society 505, no. 2 (May 31, 2021): 3041–53. http://dx.doi.org/10.1093/mnras/stab1544.
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ABSTRACT We present a detailed study of the complex time-frequency structure of a sample of previously reported bursts of FRB 121102 detected with the MeerKAT telescope in September 2019. The wide contiguous bandwidth of these observations have revealed a complex bifurcating structure in some bursts at 1250 MHz. When de-dispersed to their structure-optimized dispersion measures (DMs), two of the bursts show a clear deviation from the cold plasma dispersion relationship below 1250 MHz. We find a differential DM of ${\sim }1{-}2~{\rm pc \, cm^{-3}}$ between the lower and higher frequency regions of each burst. We investigate the possibility of plasma lensing by Gaussian lenses of ∼10 au in the host galaxy, and demonstrate that they can qualitatively produce some of the observed burst morphologies. Other possible causes for the observed frequency dependence, such as Faraday delay, are also discussed. Unresolved sub-components in the bursts, however, may have led to an incorrect DM determination. We hence advise exercising caution when considering bursts in isolation. We analyse the presence of two apparent burst pairs. One of these pairs is a potential example of upward frequency drift. The possibility that burst pairs are echoes is also discussed. The average structure-optimized DM is found to be $563.5\pm 0.2 (\text{sys}) \pm 0.8 (\text{stat})\, {\rm pc \, cm^{-3}}$ – consistent with the values reported in 2018. We use two independent methods to determine the structure-optimized DM of the bursts: the DM_phase algorithm and autocorrelation functions. The latter – originally developed for pulsar analysis – is applied to fast radio bursts for the first time in this paper.
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Pan, E., and J. L. Stringer. "Burst characteristics of dentate gyrus granule cells: evidence for endogenous and nonsynaptic properties." Journal of Neurophysiology 75, no. 1 (January 1, 1996): 124–32. http://dx.doi.org/10.1152/jn.1996.75.1.124.
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1. Hippocampal slices bathed in 8 mM potassium and 0-added calcium exhibited spontaneous epileptiform activity in the dentate gyrus. Extracellular recording revealed recurrent prolonged bursts of population spikes and an associated negative DC shift. These episodes were very similar to the in vivo phenomenon termed maximal dentate activation (MDA). Therefore this in vitro activity will be referred to as MDA-like activity or events. 2. During the MDA-like activity, the individual granule cells exhibited a sustained depolarization that matched the duration of the negative extracellular DC shift. At the beginning of the MDA-like activity, there was a burst of action potentials. After the burst, most granule cells either continued to fire action potentials regularly or in bursts. Some cells exhibited this initial burst of activity and then a dramatic reduction in firing rate. This reduction in rate was followed by a gradual increase in the amplitude and frequency of the epileptiform activity recorded during the remainder of the MDA-like event. 3. Before and between MDA-like events, spontaneous cellular activity consisted of single action potentials and bursts of action potentials on a depolarizing envelope. In addition, depolarizing potentials, up to 13 mV, were recorded. There were no extracellular field potentials associated with these intracellularly recorded potentials. 4. In the 8 mM potassium, 0-added calcium test solution, the membrane potential threshold for burst production was significantly lower than in normal potassium and calcium medium. 5. The effect of depolarizing and hyperpolarizing current injections on the amplitude and frequency of the epileptiform activity was tested. Current injection had no effect on the frequency of the epileptiform activity recorded during the MDA-like events. However, the frequency of the cellular bursts between MDA-like events was very sensitive to current injection. Depolarizing current increased the frequency, and hyperpolarizing current decreased the frequency of the spontaneous activity. 6. This study has shown that in 8 mM potassium and 0-added calcium the granule cells of the dentate gyrus are capable of generating spontaneous bursts that appear to be mediated by endogenous mechanisms. In addition, synchronized epileptiform discharges were recorded from the granule cells at regular intervals that appear were recorded from the granule cells at regular intervals that appear to be mediated by exogenous nonsynaptic mechanisms.
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Eggermont, J. J., G. M. Smith, and D. Bowman. "Spontaneous burst firing in cat primary auditory cortex: age and depth dependence and its effect on neural interaction measures." Journal of Neurophysiology 69, no. 4 (April 1, 1993): 1292–313. http://dx.doi.org/10.1152/jn.1993.69.4.1292.
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1. Neural activity was recorded with two independent electrodes separated by 0.5-2 mm, aligned in parallel, and advanced perpendicular to the surface of the cat auditory cortex. Because the experiments were part of a study into laminar interaction the difference in recording depths for the two independently movable electrodes was never > 100 microns. Multi-unit activity on each electrode was separated on-line into single-unit spike-trains with a maximum variance spike sorting algorithm. Off-line controls on the quality of the spike-train separation were routinely performed. The first aim of this study was to describe the age dependence of spontaneous burst firing and to explore if and how it could be explained by age dependent changes in firing rate. The second aim was to investigate a potential layer dependence on burst firing. The third aim was to describe the effect of burst-removal procedures on the shape, strength, and width of the cross-correlogram and to investigate whether an age dependence in burst firing might account for the previously reported age dependence in correlation strengths. 2. Recordings were made from 237 single units from primary auditory cortex in nine adult cats and from 67 units in seven kittens age 10-52 days. The incidence of burst firing as a function of firing rate, age and depth of recording and unit characteristic frequency was investigated. In addition the effect of burst firing on the strength and width of the central peak in 471 neural pair correlograms was analyzed. 3. Burst firing could be distinguished at many different time scales; bursts lasting of the order of 10 s contained bursts with durations of the order of 1 s, which in turn contained bursts of 30-50-ms duration. The analysis in this paper was restricted to the short-duration bursts. 4. Burst firing on the short-time scale of 50 ms was characterized by relatively well defined intervals between the first two spikes (3-15 ms) followed by higher-order intervals with large spread (range 4-50 ms) but with increasing modal interval value. The typical adult five-spike burst template featured spikes at 0, 3.3, 14.6, 27.2, and 34.8 ms. Burst with fewer spikes showed larger intervals between the first three spikes. 5. The probability of occurrence of isolated spikes, pairs, triplets, etc. showed a power-law dependence on firing rate with a coefficient that was significantly lower than expected under Poisson firing conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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Bikson, Marom, Rahul S. Ghai, Scott C. Baraban, and Dominique M. Durand. "Modulation of Burst Frequency, Duration, and Amplitude in the Zero-Ca2+ Model of Epileptiform Activity." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2262–70. http://dx.doi.org/10.1152/jn.1999.82.5.2262.
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Incubation of hippocampal slices in zero-Ca2+ medium blocks synaptic transmission and results in spontaneous burst discharges. This seizure-like activity is characterized by negative shifts (bursts) in the extracellular field potential and a K+ wave that propagates across the hippocampus. To isolate factors related to seizure initiation, propagation, and termination, a number of pharmacological agents were tested. K+ influx and efflux mechanisms where blocked with cesium, barium, tetraethylammonium (TEA), and 4-aminopyridine (4-AP). The effect of the gap junction blockers, heptanol and octanol, on zero-Ca2+ bursting was evaluated. Neuronal excitability was modulated with tetrodotoxin (TTX), charge screening, and applied electric fields. Glial cell function was examined with a metabolism antagonist (fluroacetate). Neuronal hyperpolarization by cation screening or applied fields decreased burst frequency but did not affect burst amplitude or duration. Heptanol attenuated burst amplitude and duration at low concentration (0.2 mM), and blocked bursting at higher concentration (0.5 mM). CsCl2 (1 mM) had no effect, whereas high concentrations (1 mM) of BaCl2 blocked bursting. TEA (25 mM) and low concentration of BaCl2 (300 μM) resulted in a two- to sixfold increase in burst duration. Fluroacetate also blocked burst activity but only during prolonged application (>3 h). Our results demonstrate that burst frequency, amplitude, and duration can be independently modulated and suggest that neuronal excitability plays a central role in burst initiation, whereas potassium dynamics establish burst amplitude and duration.
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Alessandri, Guido, Evelina De Longis, and Gianluca Cepale. "Emotional inertia emerges after prolonged states of exhaustion: Evidences from a measurement burst study." Motivation and Emotion 45, no. 4 (April 20, 2021): 518–29. http://dx.doi.org/10.1007/s11031-021-09884-4.
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AbstractExhaustion refers to the feeling of ongoing loss of emotional, physical and cognitive resources. The present study draws on the Conservation of Resources Theory to examine the relationship between chronic exhaustion and negative emotional inertia among 206 employees (aged between 19 and 50 years; M = 21.03; SD = 2.98), in a naturalistic setting. To this purpose, we used a measurement burst design with two intensive bursts—spaced 1 month apart—by repeatedly sampling exhaustion and negative affect with 18 daily diaries (a morning and an evening assessment each day) per burst. After controlling for potential confounders, results showed that exhaustion at Burst 1 predicted negative emotional inertia at Burst 2, and not the other way around. These findings advance the knowledge on the relationship between exhaustion and negative emotional inertia by providing further insights on the likely direction of causality between study variables, that is from exhaustion to inertia (but not vice versa). Practical implication, limitations, and directions for future research are also discussed.
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Badrov, Mark B., Otto F. Barak, Tanja Mijacika, Leena N. Shoemaker, Lindsay J. Borrell, Mihajlo Lojpur, Ivan Drvis, Zeljko Dujic, and J. Kevin Shoemaker. "Ventilation inhibits sympathetic action potential recruitment even during severe chemoreflex stress." Journal of Neurophysiology 118, no. 5 (November 1, 2017): 2914–24. http://dx.doi.org/10.1152/jn.00381.2017.
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This study investigated the influence of ventilation on sympathetic action potential (AP) discharge patterns during varying levels of high chemoreflex stress. In seven trained breath-hold divers (age 33 ± 12 yr), we measured muscle sympathetic nerve activity (MSNA) at baseline, during preparatory rebreathing (RBR), and during 1) functional residual capacity apnea (FRCApnea) and 2) continued RBR. Data from RBR were analyzed at matched (i.e., to FRCApnea) hemoglobin saturation (HbSat) levels (RBRMatched) or more severe levels (RBREnd). A third protocol compared alternating periods (30 s) of FRC and RBR (FRC-RBRALT). Subjects continued each protocol until 85% volitional tolerance. AP patterns in MSNA (i.e., providing the true neural content of each sympathetic burst) were studied using wavelet-based methodology. First, for similar levels of chemoreflex stress (both HbSat: 71 ± 6%; P = NS), RBRMatched was associated with reduced AP frequency and APs per burst compared with FRCApnea (both P < 0.001). When APs were binned according to peak-to-peak amplitude (i.e., into clusters), total AP clusters increased during FRCApnea (+10 ± 2; P < 0.001) but not during RBRMatched (+1 ± 2; P = NS). Second, despite more severe chemoreflex stress during RBREnd (HbSat: 56 ± 13 vs. 71 ± 6%; P < 0.001), RBREnd was associated with a restrained increase in the APs per burst (FRCApnea: +18 ± 7; RBREnd: +11 ± 5) and total AP clusters (FRCApnea: +10 ± 2; RBREnd: +6 ± 4) (both P < 0.01). During FRC-RBRALT, all periods of FRC elicited sympathetic AP recruitment (all P < 0.001), whereas all periods of RBR were associated with complete withdrawal of AP recruitment (all P = NS). Presently, we demonstrate that ventilation per se restrains and/or inhibits sympathetic axonal recruitment during high, and even extreme, chemoreflex stress. NEW & NOTEWORTHY The current study demonstrates that the sympathetic neural recruitment patterns observed during chemoreflex activation induced by rebreathing or apnea are restrained and/or inhibited by the act of ventilation per se, despite similar, or even greater, levels of severe chemoreflex stress. Therefore, ventilation modulates not only the timing of sympathetic bursts but also the within-burst axonal recruitment normally observed during progressive chemoreflex stress.
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Feng, Zhouyan, and Dominique M. Durand. "Low-Calcium Epileptiform Activity in the Hippocampus In Vivo." Journal of Neurophysiology 90, no. 4 (October 2003): 2253–60. http://dx.doi.org/10.1152/jn.00241.2003.
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It has been clearly established that nonsynaptic interactions are sufficient for generating epileptiform activity in brain slices. However, it is not known whether this type of epilepsy model can be generated in vivo. In this paper we investigate low-calcium nonsynaptic epileptiform activity in an intact hippocampus. The calcium chelator EGTA was used to lower [Ca2+]o in the hippocampus of urethane anesthetized rats. Spontaneous and evoked field potentials in CA1 pyramidal stratum and in CA1 stratum radiatum were recorded using four-channel silicon recording probes. Three different types of epileptic activity were observed while synaptic transmission was gradually blocked by a decline in hippocampal [Ca2+]o. A short latency burst, named early-burst, occurred during the early period of EGTA application. Periodic slow-waves and a long latency high-frequency burst, named late-burst, were seen after synaptic transmission was mostly blocked. Therefore these activities appear to be associated with nonsynaptic mechanisms. Moreover, the slow-waves were similar in appearance to the depolarization potential shifts in vitro with low calcium. In addition, excitatory postsynaptic amino acid antagonists could not eliminate the development of slow-waves and late-bursts. The slow-waves and late-bursts were morphologically similar to electrographic seizure activity seen in patients with temporal lobe epilepsy. These results clearly show that epileptic activity can be generated in vivo in the absence of synaptic transmission. This type of low-calcium nonsynaptic epilepsy model in an intact hippocampus could play an important role in revealing additional mechanisms of epilepsy disorders and in developing novel anti-convulsant drugs.
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Badr-El-Dine, Mohamed, George M. Gerken, and William L. Meyerhoff. "Summating Potential and Action Potential Gradients on and in the Vicinity of the round Window in Guinea Pig." Annals of Otology, Rhinology & Laryngology 106, no. 2 (February 1997): 139–44. http://dx.doi.org/10.1177/000348949710600209.
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The purpose of this study was to determine the spatial gradients of summating potential (SP) amplitudes, action potential (AP) amplitudes, and SP/AP ratios for recording loci on the round window (RW) membrane and in its vicinity. Sixteen guinea pigs were tested by means of free-field click and tone burst (2.0 kHz) stimuli. Seven recording regions were specified: five equal-area regions on the RW membrane and two basal promontory regions. Statistically significant differences were found between the promontory regions and the RW membrane regions for the SP, AP, and SP/AP obtained with click stimuli, and for the SP and AP obtained with tone burst stimuli. The SP/AP ratio for tone burst stimuli did not differ significantly across the seven regions. The RW membrane was found to be isoelectric, but there were marked spatial gradients on the basal promontory. These results are of consequence for the interpretation of transtympanic electrocochleography recordings.
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Hu, Shineng, and Alexey V. Fedorov. "Exceptionally strong easterly wind burst stalling El Niño of 2014." Proceedings of the National Academy of Sciences 113, no. 8 (February 8, 2016): 2005–10. http://dx.doi.org/10.1073/pnas.1514182113.
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Intraseasonal wind bursts in the tropical Pacific are believed to affect the evolution and diversity of El Niño events. In particular, the occurrence of two strong westerly wind bursts (WWBs) in early 2014 apparently pushed the ocean–atmosphere system toward a moderate to strong El Niño—potentially an extreme event according to some climate models. However, the event’s progression quickly stalled, and the warming remained very weak throughout the year. Here, we find that the occurrence of an unusually strong basin-wide easterly wind burst (EWB) in June was a key factor that impeded the El Niño development. It was shortly after this EWB that all major Niño indices fell rapidly to near-normal values; a modest growth resumed only later in the year. The easterly burst and the weakness of subsequent WWBs resulted in the persistence of two separate warming centers in the central and eastern equatorial Pacific, suppressing the positive Bjerknes feedback critical for El Niño. Experiments with a climate model with superimposed wind bursts support these conclusions, pointing to inherent limits in El Niño predictability. Furthermore, we show that the spatial structure of the easterly burst matches that of the observed decadal trend in wind stress in the tropical Pacific, suggesting potential links between intraseasonal wind bursts and decadal climate variations.
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Bicik, Josef, Zoran Kapelan, Christos Makropoulos, and Dragan A. Savić. "Pipe burst diagnostics using evidence theory." Journal of Hydroinformatics 13, no. 4 (November 26, 2010): 596–608. http://dx.doi.org/10.2166/hydro.2010.201.
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This paper presents a decision support methodology aimed at assisting Water Distribution System (WDS) operators in the timely location of pipe bursts. This will enable them to react more systematically and promptly. The information gathered from various data sources to help locate where a pipe burst might have occurred is frequently conflicting and imperfect. The methodology developed in this paper deals effectively with such information sources. The raw data collected in the field is first processed by means of several models, namely the pipe burst prediction model, the hydraulic model and the customer contacts model. The Dempster–Shafer Theory of Evidence is then used to combine the outputs of these models with the aim of increasing the certainty of determining the location of a pipe burst within a WDS. This new methodology has been applied to several semi-real case studies. The results obtained demonstrate that the method shows potential for locating the area of a pipe burst by capturing the varying credibility of the individual models based on their historical performance.
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Misiunas, D., J. Vítkovský, G. Olsson, M. Lambert, and A. Simpson. "Failure monitoring in water distribution networks." Water Science and Technology 53, no. 4-5 (February 1, 2006): 503–11. http://dx.doi.org/10.2166/wst.2006.154.
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An algorithm for the burst detection and location in water distribution networks based on the continuous monitoring of the flow rate at the entry point of the network and the pressure at a number of points within the network is presented. The approach is designed for medium to large bursts with opening times in the order of a few minutes and is suitable for networks of relatively small size, such as district metered areas (DMAs). The burst-induced increase in the inlet flow rate is detected using the modified cumulative sum (CUSUM) change detection test. Based on parameters obtained from the CUSUM test, the burst is simulated at a number of burst candidate locations. The calculated changes in pressure at the pressure monitoring points are then compared to the measured values and the location resulting in the best fit is selected as the burst location. The EPANET steady-state hydraulic solver is utilised to simulate the flows and pressures in the network. A sensitivity-based sampling design procedure is introduced to find the optimal positions for pressure monitoring points. The proposed algorithm is tested on a case study example network and shows potential for burst detection and location in real water distribution systems.
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White, G., D. M. Lovinger, and F. F. Weight. "Transient low-threshold Ca2+ current triggers burst firing through an afterdepolarizing potential in an adult mammalian neuron." Proceedings of the National Academy of Sciences 86, no. 17 (September 1989): 6802–6. http://dx.doi.org/10.1073/pnas.86.17.6802.
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In a variety of mammalian neurons, a brief depolarization generates an afterdepolarizing potential that triggers the firing of a short series or burst of action potentials. Although such burst firing is thought to contribute to the processing of neural information, the ionic currents that underlie this phenomenon have not been established. In whole-cell patch-clamp experiments on dorsal root ganglion neurons, we have found that the current that underlies this type of burst firing is a transient low-threshold (T-type) Ca2+ current. The data suggest that the T-type Ca2+ current may play an important role in the processing of information in the nervous system by virtue of its ability to elicit burst firing in neurons.
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Avery, Roger, and Gianluca Tosini. "Dynamics of predation in Lacertidae: the relation between locomotor pattern and prey-capture probability in three contrasted species." Amphibia-Reptilia 16, no. 1 (1995): 1–10. http://dx.doi.org/10.1163/156853895x00145.
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AbstractThe probability that lizards would capture crickets declined with distance from the snout, at rates which were significantly more rapid in all directions in Lacerta vivipara than in Podarcis muralis or L. viridis, i.e. the former species responded to potential prey over a smaller area. Capture probabilities at any distance in front of or behind the snout were lower in P. muralis or L. viridis which were pausing during locomotion than in basking lizards, confirming previous results with L. vivipara. Using capture probabilities for pausing lizards to calculate the average time it would take to find a single item of prey (tf) in relation to the mean length of locomotor bursts, on the assumption that prey could only be detected while a lizard was pausing, showed that actual mean burst distance corresponded exactly with the burst distances which gave rise to minimum tf in L. vivipara. Mean locomotor burst distances in P. muralis and L. viridis were lower than the distances which gave minimum tf values. It is suggested that, in these species, the mean burst length has evolved as a compromise between minimising tf and avoiding the high overall energy expenditures which would result from long burst lengths.
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Stewart, M., and R. K. Wong. "Intrinsic properties and evoked responses of guinea pig subicular neurons in vitro." Journal of Neurophysiology 70, no. 1 (July 1, 1993): 232–45. http://dx.doi.org/10.1152/jn.1993.70.1.232.
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1. Intracellular recordings were used to examine the membrane properties and evoked responses of subicular neurons in horizontal and parasagittal slices from guinea pig brain as a step toward understanding excitatory transmission through the hippocampus. 2. Most cells (49/74) could fire a burst discharge, a portion of which was Ca2+ dependent, in response to direct depolarization or in response to orthodromic or antidromic activation. Other cells (23/74) could not be made to burst, but instead fired single repetitive spikes when directly depolarized or single spikes in response to orthodromic or antidromic activation. Two recorded cells appeared to be interneurons and differed from bursting and non-bursting cells in action-potential shape and response to extracellular stimulation. 3. Bursting cells differed from nonbursting cells in their membrane properties: 1) their time constants were typically shorter (averaging 7.4 ms for bursting cells and 11.5 ms for nonbursting cells), 2) they exhibited a pronounced "sag" in the potential response to hyperpolarizing current injection, and 3) they responded at the break of a hyperpolarizing stimulus with a depolarization (anodal break potential). The sag and the anodal break potential were not detected in recordings from nonbursting neurons. 4. A single-spiking mode could be induced in bursting cells by depolarization from resting potential to about -60 mV. Conversely, hyperpolarization of nonbursting cells did not convert them to bursting cells. 5. Both bursting and nonbursting cell types could be antidromically driven. Whereas both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) were prominent in nonbursting cells, IPSPs were observed at a lower stimulus intensities than EPSPs in most cells. EPSPs were evident in bursting cells and they triggered burst discharges. IPSPs in bursting cells were detected only when these cells were depolarized, eliminating burst responses. 6. Spontaneous firing rates were low (averaging < 1 spike/s) for both cell types. Addition of picrotoxin produced spontaneous burst or EPSP responses in bursting cells, synchronous with different patterns of picrotoxin-induced population bursts originating in CA3 and/or entorhinal cortex. Individual subicular cells followed CA3 or entorhinal cortex or both. No such activity was recorded in nonbursting cells. No increases in activity in either cell type were seen after picrotoxin application to isolated pieces of subicular cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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Deng, Lin, Yan Lv, and Rong Gui Deng. "New Rock Burst Prediction Method." Advanced Materials Research 446-449 (January 2012): 762–66. http://dx.doi.org/10.4028/www.scientific.net/amr.446-449.762.
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This paper gives a new rock burst prediction method of potential index, according to the rock deformation and failure of the rock and the relationship between energy transfer, the characteristics of uniaxial compression stress-strain entire process curve. The new prediction method of rock burst of energy with existing method for forecasting index was compared and analyzed. Testing study was made on the typical rocks of rhyolite, from the deep deposit of Niba mountain tunnel, Combined with the actual phenomen of rock burst, the rock burst potential index is verified to be able to show fairly well the rock burst proneness. Finally, a criterion of rock burst proneness is put forward.
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Vignesh, Sangu Srinivasan, Niraj Kumar Singh, and Krishna Rajalakshmi. "Tone Burst Masseter Vestibular Evoked Myogenic Potentials: Normative Values and Test–Retest Reliability." Journal of the American Academy of Audiology 32, no. 05 (May 2021): 308–14. http://dx.doi.org/10.1055/s-0041-1728718.
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Abstract Background Masseter vestibular evoked myogenic potential (mVEMP) is a recent tool for the assessment of vestibular and trigeminal pathways. Though a few studies have recorded mVEMP using click stimuli, there are no reports of these potentials using the more conventional VEMP eliciting stimuli, the tone bursts. Purpose The aim of the study is to establish normative values and determine the test–retest reliability of tone burst evoked mVEMP. Research Design The research design type is normative study design. Study Sample Forty-four healthy participants without hearing and vestibular deficits in the age range of 18 to 50 years participated in the study. Data Collection and Analysis All participants underwent mVEMP testing using 500 Hz tone-burst stimuli at 125 dB peSPL. Ten participants underwent second mVEMP testing within 1 month of the initial testing to estimate the test–retest reliability. Results Tone burst mVEMP showed robust responses in all participants. There were no significant ear and sex differences on any mVEMP parameter (p > 0.05); however, males had significantly higher EMG normalized peak-to-peak amplitude than females. Intraclass correlation coefficient (ICC) values of tone burst mVEMP showed excellent test–retest reliability (ICC >0.75) for ipsilateral and contralateral p11 latency, ipsilateral EMG normalized p11-n21 peak to peak amplitude, and amplitude asymmetry ratio. Fair and good test–retest reliability (0.4 < ICC > 0.75) was observed for ipsilateral and contralateral n21 latency, contralateral EMG normalized peak-to-peak amplitude, and amplitude asymmetry ratio. Conclusion Tone burst mVEMP is a robust and reliable test for evaluating the functional integrity of the vestibulomasseteric reflex pathway.
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Phares, Gregg A., and John H. Byrne. "Analysis of 5-HT–Induced Short-Term Facilitation at Aplysia Sensorimotor Synapse During Bursts: Increased Synaptic Gain That Does Not Require ERK Activation." Journal of Neurophysiology 94, no. 1 (July 2005): 871–77. http://dx.doi.org/10.1152/jn.01261.2004.
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The 5-HT–induced synaptic plasticity of Aplysia sensorimotor synapses has typically been probed by firing a single presynaptic spike. In this study, 5-HT–induced synaptic plasticity was probed with brief bursts of spikes (10 Hz, 1 s), which are more behaviorally relevant stimuli. Because such bursts provide a greater challenge to the release machinery than single spikes, their use may reveal additional aspects of synaptic modulation, and, in particular, the role of extracellular signal-regulated protein kinase (ERK), which has recently been implicated in several examples of short- and long-term synaptic plasticity. Excitatory postsynaptic currents (EPSCs) were characterized by their amplitudes. In addition, two kinetic measurements, time to peak and decay time constant, were determined for the initial and last EPSCs of each burst. Application of 5-HT produced a uniform increase in gain by facilitating each EPSC elicited during a burst of spikes without affecting the kinetics of the initial or last EPSC. These data suggest that short-term facilitation during a burst is mediated largely by processes such as those that affect the size of the releasable pool or rate of vesicle mobilization rather than by an increase in the duration of the presynaptic action potential. An ERK cascade inhibitor (U0126) had no effect on the 5-HT–mediated facilitation of either the initial EPSC or EPSCs elicited late in the burst.
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Staff, Nathan P., Hae-Yoon Jung, Tara Thiagarajan, Michael Yao, and Nelson Spruston. "Resting and Active Properties of Pyramidal Neurons in Subiculum and CA1 of Rat Hippocampus." Journal of Neurophysiology 84, no. 5 (November 1, 2000): 2398–408. http://dx.doi.org/10.1152/jn.2000.84.5.2398.
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Action potentials are the end product of synaptic integration, a process influenced by resting and active neuronal membrane properties. Diversity in these properties contributes to specialized mechanisms of synaptic integration and action potential firing, which are likely to be of functional significance within neural circuits. In the hippocampus, the majority of subicular pyramidal neurons fire high-frequency bursts of action potentials, whereas CA1 pyramidal neurons exhibit regular spiking behavior when subjected to direct somatic current injection. Using patch-clamp recordings from morphologically identified neurons in hippocampal slices, we analyzed and compared the resting and active membrane properties of pyramidal neurons in the subiculum and CA1 regions of the hippocampus. In response to direct somatic current injection, three subicular firing types were identified (regular spiking, weak bursting, and strong bursting), while all CA1 neurons were regular spiking. Within subiculum strong bursting neurons were found preferentially further away from the CA1 subregion. Input resistance ( R N), membrane time constant (τm), and depolarizing “sag” in response to hyperpolarizing current pulses were similar in all subicular neurons, while R N and τm were significantly larger in CA1 neurons. The first spike of all subicular neurons exhibited similar action potential properties; CA1 action potentials exhibited faster rising rates, greater amplitudes, and wider half-widths than subicular action potentials. Therefore both the resting and active properties of CA1 pyramidal neurons are distinct from those of subicular neurons, which form a related class of neurons, differing in their propensity to burst. We also found that both regular spiking subicular and CA1 neurons could be transformed into a burst firing mode by application of a low concentration of 4-aminopyridine, suggesting that in both hippocampal subfields, firing properties are regulated by a slowly inactivating, D-type potassium current. The ability of all subicular pyramidal neurons to burst strengthens the notion that they form a single neuronal class, sharing a burst generating mechanism that is stronger in some cells than others.
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Lintunen, Anna, Adriano Losso, Juho Aalto, Tommy Chan, Teemu Hölttä, and Stefan Mayr. "Propagating ice front induces gas bursts and ultrasonic acoustic emissions from freezing xylem." Tree Physiology 40, no. 2 (December 19, 2019): 170–82. http://dx.doi.org/10.1093/treephys/tpz123.
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Abstract Ice formation and propagation in the xylem of plants is a complex process. During freezing of xylem sap, gases dissolved in liquid sap are forced out of the ice lattice due to their low solubility in ice, and supersaturation of xylem sap as well as low water potential (Ѱ) are induced at the ice–liquid interface. Supersaturation of gases near the ice front may lead to bubble formation and potentially to cavitation and/or to burst of gases driven out from the branch. In this study, we investigated the origin and dynamics of freezing-related gas bursts and ultrasonic acoustic emissions (AEs), which are suggested to indicate cavitation. Picea abies (L.) H. Karst. and Salix caprea L. branch segments were exposed to frost cycles in a temperature test chamber, and CO2 efflux (indicating gas bursts) and AEs were recorded. On freezing, two-thirds of the observed gas bursts originated from the xylem and only one-third from the bark. Simultaneously with gas bursts, AEs were detected. Branch Ѱ affected both gas bursts and AEs, with high gas burst in saturated and dry samples but relevant AEs only in the latter. Repeated frost cycles led to decreasing gas burst volumes and AE activity. Experiments revealed that the expanding ice front in freezing xylem was responsible for observed gas bursts and AEs, and that branch Ѱ influenced both processes. Results also indicated that gas bursts and cavitation are independently induced by ice formation, though both may be relevant for bubble dynamics during freezing.
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Pleunis, Ziggy, Deborah C. Good, Victoria M. Kaspi, Ryan Mckinven, Scott M. Ransom, Paul Scholz, Kevin Bandura, et al. "Fast Radio Burst Morphology in the First CHIME/FRB Catalog." Astrophysical Journal 923, no. 1 (December 1, 2021): 1. http://dx.doi.org/10.3847/1538-4357/ac33ac.
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Abstract We present a synthesis of fast radio burst (FRB) morphology (the change in flux as a function of time and frequency) as detected in the 400–800 MHz octave by the FRB project on the Canadian Hydrogen Intensity Mapping Experiment (CHIME/FRB), using events from the first CHIME/FRB catalog. The catalog consists of 62 bursts from 18 repeating sources, plus 474 one-off FRBs, detected between 2018 July 25 and 2019 July 2. We identify four observed archetypes of burst morphology (“simple broadband,” “simple narrowband,” “temporally complex,” and “downward drifting”) and describe relevant instrumental biases that are essential for interpreting the observed morphologies. Using the catalog properties of the FRBs, we confirm that bursts from repeating sources, on average, have larger widths, and we show, for the first time, that bursts from repeating sources, on average, are narrower in bandwidth. This difference could be due to beaming or propagation effects, or it could be intrinsic to the populations. We discuss potential implications of these morphological differences for using FRBs as astrophysical tools.
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Aloy, Miguel A. "The First Steps in the Life of a GRB." International Astronomical Union Colloquium 192 (2005): 483–89. http://dx.doi.org/10.1017/s025292110000957x.
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SummaryWe present some preliminary results of relativistic hydrodynamic simulations of post-neutron star merger disks as potential candidates for progenitors of short-lasting gamma-ray bursts. We discuss some of the generic conditions under which a gamma-ray burst can be initiated in this kind of progenitor and the main characteristics of the resulting outflow.
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Magee, Jeffrey C., and Michael Carruth. "Dendritic Voltage-Gated Ion Channels Regulate the Action Potential Firing Mode of Hippocampal CA1 Pyramidal Neurons." Journal of Neurophysiology 82, no. 4 (October 1, 1999): 1895–901. http://dx.doi.org/10.1152/jn.1999.82.4.1895.
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The role of dendritic voltage-gated ion channels in the generation of action potential bursting was investigated using whole cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons located in hippocampal slices of adult rats. Under control conditions somatic current injections evoked single action potentials that were associated with an afterhyperpolarization (AHP). After localized application of 4-aminopyridine (4-AP) to the distal apical dendritic arborization, the same current injections resulted in the generation of an afterdepolarization (ADP) and multiple action potentials. This burst firing was not observed after localized application of 4-AP to the soma/proximal dendrites. The dendritic 4-AP application allowed large-amplitude Na+-dependent action potentials, which were prolonged in duration, to backpropagate into the distal apical dendrites. No change in action potential backpropagation was seen with proximal 4-AP application. Both the ADP and action potential bursting could be inhibited by the bath application of nonspecific concentrations of divalent Ca2+ channel blockers (NiCl and CdCl). Ca2+ channel blockade also reduced the dendritic action potential duration without significantly affecting spike amplitude. Low concentrations of TTX (10–50 nM) also reduced the ability of the CA1 neurons to fire in the busting mode. This effect was found to be the result of an inhibition of backpropagating dendritic action potentials and could be overcome through the coordinated injection of transient, large-amplitude depolarizing current into the dendrite. Dendritic current injections were able to restore the burst firing mode (represented as a large ADP) even in the presence of high concentrations of TTX (300–500 μM). These data suggest the role of dendritic Na+ channels in bursting is to allow somatic/axonal action potentials to backpropagate into the dendrites where they then activate dendritic Ca2+ channels. Although it appears that most Ca2+ channel subtypes are important in burst generation, blockade of T- and R-type Ca2+ channels by NiCl (75 μM) inhibited action potential bursting to a greater extent than L-channel (10 μM nimodipine) or N-, P/Q-type (1 μM ω-conotoxin MVIIC) Ca2+ channel blockade. This suggest that the Ni-sensitive voltage-gated Ca2+ channels have the most important role in action potential burst generation. In summary, these data suggest that the activation of dendritic voltage-gated Ca2+ channels, by large-amplitude backpropagating spikes, provides a prolonged inward current that is capable of generating an ADP and burst of multiple action potentials in the soma of CA1 pyramidal neurons. Dendritic voltage-gated ion channels profoundly regulate the processing and storage of incoming information in CA1 pyramidal neurons by modulating the action potential firing mode from single spiking to burst firing.
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Mattia, D., G. G. Hwa, and M. Avoli. "Membrane properties of rat subicular neurons in vitro." Journal of Neurophysiology 70, no. 3 (September 1, 1993): 1244–48. http://dx.doi.org/10.1152/jn.1993.70.3.1244.
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1. Conventional intracellular recordings were performed in rat hippocampal slices to investigate the electrophysiological properties of subicular neurons. These cells had a resting membrane potential (RMP) of -66 +/- 7.2 mV (mean +/- SD; n = 50), input resistance of 23.6 +/- 8.2 M omega (n = 51), time constant of 7.1 +/- 1.9 ms (n = 51), action potential amplitude of 85.8 +/- 13.8 mV (n = 50), and duration of 2.9 +/- 1.2 ms (n = 48). Analysis of the current-voltage relationship revealed membrane inward rectification in both depolarizing and hyperpolarizing direction. The latter type was readily abolished by Cs+ (3 mM; n = 6 cells). 2. Injection of depolarizing current pulses of threshold intensity induced in all subicular neurons (n = 51) recorded at RMP a burst of two to three fast action potentials (frequency = 212.7 +/- 90 Hz, n = 13 cells). This burst rode on a slow depolarizing envelope and was followed by an afterhyperpolarization and later by regular spiking mode once the pulse was prolonged. Similar bursts were also generated upon termination of a hyperpolarizing current pulse. 3. The slow depolarization underlying the burst resembled a low-threshold response, which in thalamic cells is caused by a Ca2+ conductance and is contributed by the Cs(+)-sensitive inward rectifier. However, bursts in subicular cells persisted in medium containing the Ca(2+)-channel blockers Co2+ (2 mM) and Cd2+ (1 mM) (n = 5 cells) but disappeared during application of TTX (1 microM; n = 3 cells). Hence they were mediated by Na+. Blockade of the hyperpolarizing inward rectification by Cs+ did not prevent the rebound response (n = 3 cells). 4. Our findings demonstrate that intrinsic bursts, presumably related to a "low-threshold" Na+ conductance are present in rat subicular neurons. Similar intrinsic characteristics have been suggested to underlie the rhythmic activity described in other neuronal networks, although in most cases the low-threshold electrogenesis was caused by Ca2+. We propose that the bursting mechanism might play a role in modulating incoming signals from the classical hippocampal circuit within the limbic system.
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Opitz, Thoralf, Ana D. De Lima, and Thomas Voigt. "Spontaneous Development of Synchronous Oscillatory Activity During Maturation of Cortical Networks In Vitro." Journal of Neurophysiology 88, no. 5 (November 1, 2002): 2196–206. http://dx.doi.org/10.1152/jn.00316.2002.
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Recent studies have focused attention on mechanisms of spontaneous large-scale wavelike activity during early development of the neocortex. In this study, we describe and characterize synchronous neuronal activity that occurs in cultured cortical networks naturally without pharmacological intervention. The synchronous activity that can be detected by means of Fluo-3 fluorescence imaging starts to develop at the beginning of the second week in culture and eventually includes the entire neuronal population about 1 wk later. A synchronous increase of [Ca2+]i in the neuronal population is associated with a burst of action potentials riding on a long-lasting depolarization recorded in a single cell. It is suggested that this depolarization results directly from synaptic current, which was comprised of at least three different components mediated by AMPA, N-methyl-d-aspartate (NMDA), and GABAA receptors. We never observed a gradually depolarizing pacemaker potential and found no evidence for a change of excitability during inter-burst periods. However, we found evidence for a period of synaptic depression after bursts. Network excitability recovers gradually over seconds from this depression that can explain the episodic nature of spontaneous network activity. Using pharmacological manipulation to investigate the propagation of activity in the network, we show that synchronous network activity depends on both glutamatergic and GABAAergic neurotransmission during a brief period. Reversal potential of GABAA receptor-mediated current was found to be significantly more positive than resting membrane potential both at 1 and 2 wk in culture, suggesting depolarizing action of GABA. However, in cultures older than 2 wk, inhibition of GABAAreceptors does not result in block of synchronous network activity but in modulation of burst width and frequency.