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Journal articles on the topic 'Depolarization wave propagation'
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Ben-Shimol, Y., N. Blaunstein, and M. Sergeev. "DEPOLARIZATION EFFECTS OF RADIO WAVE PROPAGATION IN VARIOUS LAND BUILT–UP ENVIRONMENTS." Informatsionno-upravliaiushchie sistemy (Information and Control Systems) 74, no. 1 (February 2015): 68–76. http://dx.doi.org/10.15217/issn1684-8853.2015.1.68.
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Momose-Sato, Yoko, Naohisa Miyakawa, Hiraku Mochida, Shinichi Sasaki, and Katsushige Sato. "Optical Analysis of Depolarization Waves in the Embryonic Brain: A Dual Network of Gap Junctions and Chemical Synapses." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 600–614. http://dx.doi.org/10.1152/jn.00337.2002.
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Correlated neuronal activity plays a fundamental role in the development of the CNS. Using a multiple-site optical recording technique with a voltage-sensitive dye, we previously described a novel type of depolarization wave that was evoked by cranial or spinal nerve stimulation and spread widely over the whole brain region in the chick embryo. We have now investigated developmental expression and neuronal network mechanisms of this depolarization wave by applying direct stimulation to the brain stem or upper cervical cord of E5–E11 embryos, which elicited wave activity similar to that evoked by nerve stimulation. Spatial distribution patterns of the depolarization wave changed dynamically with development, and this change appeared to be related to the regional differences in neuronal differentiation. The depolarization wave was completely eliminated by application of either gap junction blockers or an N-methyl-d-aspartate (NMDA)-receptor antagonist, indicating that functions of both gap junctions and NMDA receptors are indispensable for wave propagation. A possible interpretation of the results is that dual networks of gap junctions and chemical synaptic coupling mediate large-scale depolarization waves in the developing chick CNS.
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Santos, Edgar, Renán Sánchez-Porras, Oliver W. Sakowitz, Jens P. Dreier, and Markus A. Dahlem. "Heterogeneous propagation of spreading depolarizations in the lissencephalic and gyrencephalic brain." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (January 25, 2017): 2639–43. http://dx.doi.org/10.1177/0271678x16689801.
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In the recently published article, “Heterogeneous incidence and propagation of spreading depolarizations,” it is shown, in vivo and in vitro, how KCl-induced spreading depolarizations in mouse and rat brains can be highly variable, and that they are not limited, as once thought, to a concentric, isotropic, or homogenous depolarization wave in space or in time. The reported results serve as a link between the different species, and this paper contributes to changing the way in which SD expansion is viewed in the lissencephalic brain. Here, we discuss their results with our previous observations made in the gyrencephalic swine brain, in computer simulations, and in the human brain.
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Bayguinov, Orline, Sean M. Ward, James L. Kenyon, and Kenton M. Sanders. "Voltage-gated Ca2+ currents are necessary for slow-wave propagation in the canine gastric antrum." American Journal of Physiology-Cell Physiology 293, no. 5 (November 2007): C1645—C1659. http://dx.doi.org/10.1152/ajpcell.00165.2007.
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Electrical slow waves determine the timing and force of peristaltic contractions in the stomach. Slow waves originate from a dominant pacemaker in the orad corpus and propagate actively around and down the stomach to the pylorus. The mechanism of slow-wave propagation is controversial. We tested whether Ca2+ entry via a voltage-dependent, dihydropyridine-resistant Ca2+ conductance is necessary for active propagation in canine gastric antral muscles. Muscle strips cut parallel to the circular muscle were studied with intracellular electrophysiological techniques using a partitioned-chamber apparatus. Slow-wave upstroke velocity and plateau amplitude decreased from the greater to the lesser curvature, and this corresponded to a decrease in the density of interstitial cells of Cajal in the lesser curvature. Slow-wave propagation velocity between electrodes impaling cells in two regions of muscle and slow-wave upstroke and plateau were measured in response to experimental conditions that reduce the driving force for Ca2+ entry or block voltage-dependent Ca2+ currents. Nicardipine (0.1–1 μM) did not affect slow-wave upstroke or propagation velocities. Upstroke velocity, amplitude, and propagation velocity were reduced in a concentration-dependent manner by Ni2+ (1–100 μM), mibefradil (10–30 μM), and reduced extracellular Ca2+ (0.5–1.5 mM). Depolarization (by 10–15 mM K+) or hyperpolarization (10 μM pinacidil) also reduced upstroke and propagation velocities. The higher concentrations (or lowest Ca2+) of these drugs and ionic conditions tested blocked slow-wave propagation. Treatment with cyclopiazonic acid to empty Ca2+ stores did not affect propagation. These experiments show that voltage-dependent Ca2+ entry is obligatory for the upstroke phase of slow waves and active propagation.
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Tryba, Andrew K., Edward M. Merricks, Somin Lee, Tuan Pham, SungJun Cho, Douglas R. Nordli, Tahra L. Eissa, et al. "Role of paroxysmal depolarization in focal seizure activity." Journal of Neurophysiology 122, no. 5 (November 1, 2019): 1861–73. http://dx.doi.org/10.1152/jn.00392.2019.
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We analyze the role of inhibition in sustaining focal epileptic seizure activity. We review ongoing seizure activity at the mesoscopic scale that can be observed with microelectrode arrays as well as at the macroscale of standard clinical EEG. We provide clinical, experimental, and modeling data to support the hypothesis that paroxysmal depolarization (PD) is a critical component of the ictal machinery. We present dual-patch recordings in cortical cultures showing reduced synaptic transmission associated with presynaptic occurrence of PD, and we find that the PD threshold is cell size related. We further find evidence that optically evoked PD activity in parvalbumin neurons can promote propagation of neuronal excitation in neocortical networks in vitro. Spike sorting results from microelectrode array measurements around ictal wave propagation in human focal seizures demonstrate a strong increase in putative inhibitory firing with an approaching excitatory wave, followed by a sudden reduction of firing at passage. At the macroscopic level, we summarize evidence that this excitatory ictal wave activity is strongly correlated with oscillatory activity across a centimeter-sized cortical network. We summarize Wilson–Cowan-type modeling showing how inhibitory function is crucial for this behavior. Our findings motivated us to develop a network motif of neurons in silico, governed by a reduced version of the Hodgkin–Huxley formalism, to show how feedforward, feedback, PD, and local failure of inhibition contribute to observed dynamics across network scales. The presented multidisciplinary evidence suggests that the PD not only is a cellular marker or epiphenomenon but actively contributes to seizure activity. NEW & NOTEWORTHY We present mechanisms of ongoing focal seizures across meso- and macroscales of microelectrode array and standard clinical recordings, respectively. We find modeling, experimental, and clinical evidence for a dual role of inhibition across these scales: local failure of inhibition allows propagation of a mesoscopic ictal wave, whereas inhibition elsewhere remains intact and sustains macroscopic oscillatory activity. We present evidence for paroxysmal depolarization as a mechanism behind this dual role of inhibition in shaping ictal activity.
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Smith, T. K., J. B. Reed, and K. M. Sanders. "Effects of membrane potential on electrical slow waves of canine proximal colon." American Journal of Physiology-Cell Physiology 255, no. 6 (December 1, 1988): C828—C834. http://dx.doi.org/10.1152/ajpcell.1988.255.6.c828.
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The effects of membrane potential on the waveforms and propagation of slow waves were tested using circular muscles of the canine colon. Studies were conducted with intracellular recording techniques on cross-sectional strips of canine proximal colon. Circular muscle cells near the submucosa generated slow waves that decayed in amplitude as they spread through the circular layer. The membrane potentials of cells were less negative as a function of distance from the submucosal border. Cells near the submucosa were depolarized with elevated external K+ and electrical pulses using the partitioned chamber technique. The waveforms of depolarized submucosal cells were compared with events recorded from cells in the bulk of the circular layer. The waveform changes caused by experimental depolarization were different from the changes in waveform that occur during propagation, suggesting the latter are due to a different mechanism than depolarization. The effects of the membrane potential on syncytial input resistance and length constant were also evaluated. The results of these studies are consistent with the hypothesis that slow-wave propagation across the circular layer in canine proximal colon occurs passively.
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Seppey, Dominique, Roger Sauser, Michèle Koenigsberger, Jean-Louis Bény, and Jean-Jacques Meister. "Intercellular calcium waves are associated with the propagation of vasomotion along arterial strips." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 2 (February 2010): H488—H496. http://dx.doi.org/10.1152/ajpheart.00281.2009.
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Vasomotion consists of cyclic arterial diameter variations induced by synchronous contractions and relaxations of smooth muscle cells. However, the arteries do not contract simultaneously on macroscopic distances, and a propagation of the contraction can be observed. In the present study, our aim was to investigate this propagation. We stimulated endothelium-denuded rat mesenteric arterial strips with phenylephrine (PE) to obtain vasomotion and observed that the contraction waves are linked to intercellular calcium waves. A velocity of ∼100 μm/s was measured for the two kinds of waves. To investigate the calcium wave propagation mechanisms, we used a method allowing a PE stimulation of a small area of the strip. No calcium propagation could be induced by this local stimulation when the strip was in its resting state. However, if a low PE concentration was added on the whole strip, local PE stimulations induced calcium waves, spreading over finite distances. The calcium wave velocity induced by local stimulation was identical to the velocity observed during vasomotion. This suggests that the propagation mechanisms are similar in the two cases. Using inhibitors of gap junctions and of voltage-operated calcium channels, we showed that the locally induced calcium propagation likely depends on the propagation of the smooth muscle cell depolarization. Finally, we proposed a model of the propagation mechanisms underlying these intercellular calcium waves.
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Kwaku, Kevin F., and Stephen M. Dillon. "Shock-Induced Depolarization of Refractory Myocardium Prevents Wave-Front Propagation in Defibrillation." Circulation Research 79, no. 5 (November 1996): 957–73. http://dx.doi.org/10.1161/01.res.79.5.957.
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Blackwell, K. T. "Calcium Waves and Closure of Potassium Channels in Response to GABA Stimulation in Hermissenda Type B Photoreceptors." Journal of Neurophysiology 87, no. 2 (February 1, 2002): 776–92. http://dx.doi.org/10.1152/jn.00867.2000.
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Classical conditioning of Hermissenda crassicornisrequires the paired presentation of a conditioned stimulus (light) and an unconditioned stimulus (turbulence). Light stimulation of photoreceptors leads to production of diacylglycerol, an activator of protein kinase C, and inositol triphosphate (IP3), which releases calcium from intracellular stores. Turbulence causes hair cells to release GABA onto the terminal branches of the type B photoreceptor. One prior study has shown that GABA stimulation produces a wave of calcium that propagates from the terminal branches to the soma and raises the possibility that two sources of calcium are required for memory storage. GABA stimulation also causes an inhibitory postsynaptic potential (IPSP) followed by a late depolarization and increase in input resistance, whose cause has not been identified. A model was developed of the effect of GABA stimulation on the Hermissenda type B photoreceptor to evaluate the currents underlying the late depolarization and to evaluate whether a calcium wave could propagate from the terminal branches to the soma. The model included GABAA, GABAB, and calcium-sensitive potassium leak channels; calcium dynamics including release of calcium from intracellular stores; and the biochemical reactions leading from GABAB receptor activation to IP3 production. Simulations show that it is possible for a wave of calcium to propagate from the terminal branches to the soma. The wave is initiated by IP3-induced calcium release but propagation requires release through the ryanodine receptor channel where IP3 concentration is small. Wave speed is proportional to peak calcium concentration at the crest of the wave, with a minimum speed of 9 μm/s in the absence of IP3. Propagation ceases when peak concentration drops below 1.2 μM; this occurs if the rate of calcium pumping into the endoplasmic reticulum is too large. Simulations also show that both a late depolarization and an increase in input resistance occur after GABA stimulation. The duration of the late depolarization corresponds to the duration of potassium leak channel closure. Neither the late depolarization nor the increase in input resistance are observed when a transient calcium current and a hyperpolarization-activated current are added to the model as replacement for closure of potassium leak channels. Thus the late depolarization and input resistance elevation can be explained by a closure of calcium-sensitive leak potassium currents but cannot be explained by a transient calcium current and a hyperpolarization-activated current.
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Senseman, David M., and Kay A. Robbins. "High-Speed VSD Imaging of Visually Evoked Cortical Waves: Decomposition Into Intra- and Intercortical Wave Motions." Journal of Neurophysiology 87, no. 3 (March 1, 2002): 1499–514. http://dx.doi.org/10.1152/jn.00475.2001.
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In the pond turtle, Pseudemys scripta elegans, visually evoked cortical waves propagate at different velocities within the primary visual area compared with waves that pass into the secondary visual area. In an effort to separate intra- and intercortical wave motions, movies of visually evoked cortical waves recorded by high-speed voltage-sensitive dye (VSD) imaging were subjected to Karhunen-Loéve (KL) decomposition. This procedure decomposes the VSD movies into a series of basis images that capture different spatial patterns of coherent activity. Most of the energy of the compound wave motion (>95%) was captured by the three largest basis images, M1,1 , M1,2 , and M2,1 . Based on visual comparison with maps of wave front latency, KL basis image M1,2 appears to capture the spread of depolarization within the primary visual area, whereas KL basis image M2,1 appears to capture the spread of depolarization from the primary into the secondary visual area. The contribution of different basis images to the intra- and intercortical wave motions was tested by reconstructing the response using different combinations of KL basis images. Only KL basis images M1,1 and M1,2 were needed to reconstruct intracortical wave motion, while basis images M1,1 and M2,1 were needed to reconstruct intercortical wave motion. It was also found that the direction and speed of wave propagation could be deduced by visual inspection of the basis image projections on to the original data set. The relative advantage of KL decomposition for the analysis of complex wave motions captured by VSD imaging is discussed.
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Aiba, Isamu, Andrew P. Carlson, Christian T. Sheline, and C. William Shuttleworth. "Synaptic release and extracellular actions of Zn2+ limit propagation of spreading depression and related events in vitro and in vivo." Journal of Neurophysiology 107, no. 3 (February 2012): 1032–41. http://dx.doi.org/10.1152/jn.00453.2011.
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Cortical spreading depression (CSD) is a consequence of a slowly propagating wave of neuronal and glial depolarization (spreading depolarization; SD). Massive release of glutamate contributes to SD propagation, and it was recently shown that Zn2+ is also released from synaptic vesicles during SD. The present study examined consequences of extracellular Zn2+ accumulation on the propagation of SD. SD mechanisms were studied first in murine brain slices, using focal KCl applications as stimuli and making electrical and optical recordings in hippocampal area CA1. Elevating extracellular Zn2+ concentrations with exogenous ZnCl2 reduced SD propagation rates. Selective chelation of endogenous Zn2+ (using TPEN or CaEDTA) increased SD propagation rates, and these effects appeared due to chelation of Zn2+ derived from synaptic vesicles. Thus, in tissues where synaptic Zn2+ release was absent [knockout (KO) of vesicular Zn2+ transporter ZnT-3], SD propagation rates were increased, and no additional increase was observed following chelation of endogenous Zn2+ in these tissues. The role of synaptic Zn2+ was then examined on CSD in vivo. ZnT-3 KO animals had higher susceptibility to CSD than wild-type controls as evidenced by significantly higher propagation rates and frequencies. Studies of candidate mechanisms excluded changes in neuronal excitability, presynaptic release, and GABA receptors but left open a possible contribution of N-methyl-d-aspartate (NMDA) receptor inhibition. These results suggest the extracellular accumulation of synaptically released Zn2+ can serve as an intrinsic inhibitor to limit SD events. The inhibitory action of extracellular Zn2+ on SD may counteract to some extent the neurotoxic effects of intracellular Zn2+ accumulation in acute brain injury models.
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Jiang, Dong Dong, Jin Mei Du, Yan Gu, and Yu Jun Feng. "Electrical Behavior of PSZT Ferroelectric Ceramic under Shock Wave Compression." Key Engineering Materials 368-372 (February 2008): 21–23. http://dx.doi.org/10.4028/www.scientific.net/kem.368-372.21.
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Electric power of hundreds of kilowatts can be produced in a few microseconds by sudden release of bound charge on the surface of ferroelectric ceramic through shock wave compression. In order to understand the depolarization process, knowledge of the discharge behavior of ferroelectric ceramic under shock wave compression is essential. Gas-gun facility has been used to investigate the shock-induced depolarization kinetics of tin-modified lead zirconate titanate ferroelectric ceramic. Experiments were conducted in the normal mode in which the shock propagation vector was perpendicular to the remanent polarization. Two kinds of specimens with the ferroelectric-toantiferroelectric transformation hydraulic pressure respectively at 80 MPa and 180 MPa were tested. The output currents as a function of load resistance were measured. A computation model was developed to describe the electrical behavior of PSZT ceramic under shock wave compression, which adequately explained the observed experimental results.
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Jasiūnienė, Elena, Egidijus Žukauskas, and Rymantas Kažys. "Numerical Investigation of Propagation of Ultrasonic Waves in the Waveguides with Mode Conversion." Key Engineering Materials 543 (March 2013): 219–22. http://dx.doi.org/10.4028/www.scientific.net/kem.543.219.
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Ultrasonic investigation techniques are widely used in materials characterisation and non-destructive testing applications. In special cases of applications, such as investigation of properties of melted polymers, metals and hot liquids, measurements must be performed in a wide temperature range. However conventional piezoelectric transducers cannot withstand higher temperatures than the Curie temperature. Therefore in order to protect conventional ultrasonic transducers from influence of a high temperature and to avoid depolarization, measurements must be performed using special waveguides with a low thermal conductivity between the object under investigation and the ultrasonic transducer. For measurements of the material properties, such as viscoelastic properties of materials, additional shear wave transducers must be used. In this work approach how to excite both, longitudinal and shear waves using special waveguides with mode conversion, using pair of conventional ultrasonic longitudinal wave transducers is presented. In this work numerical investigation of propagation of longitudinal and shear ultrasonic waves in the waveguides with mode conversion using finite element method and CIVA software was carried out. Modelling of propagation of simultaneously generated longitudinal and shear waves using pair of longitudinal ultrasonic transducers was performed. Influence of temperature gradient to the required incidence angle of the longitudinal wave was evaluated.
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Momose-Sato, Yoko, Yoshiko Honda, Hiroshi Sasaki, and Katsushige Sato. "Optical Imaging of Large-Scale Correlated Wave Activity in the Developing Rat CNS." Journal of Neurophysiology 94, no. 2 (August 2005): 1606–22. http://dx.doi.org/10.1152/jn.00044.2005.
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Correlated neuronal activity plays a fundamental role in the development of the nervous system. Using a multiple-site optical recording technique with a fast voltage-sensitive dye, we previously reported a novel form of correlated activity in the chick embryo, which showed wide propagation throughout the CNS. In this study, we report that similar wave activity is generated in the embryonic rat CNS. Electrical stimulation applied to the cervical cord evoked wave activity that traveled over a wide region of the CNS including the medulla, pons, midbrain, diencephalon, and spinal cord. Small signals were also detected from the cerebellum and part of the cerebrum. Stimulation applied to the cranial nerves such as the trigeminal and vagus nerves evoked waves with similar patterns, indicating that the wave is triggered by external sensory inputs. This wave activity was inhibited by glutamate-, acetylcholine-, GABA- and glycine-receptor antagonists in addition to gap junction blockers such as octanol and 18β-glycyrrhetinic acid. In the immunohistochemical study, significant immunoreactivity of connexin26 and connexin32 was also observed. Wave activity detected with a voltage-sensitive dye was accompanied by a Ca2+-wave, indicating that it not only provides electrical synchrony but also biochemical signals associated with [Ca2+]i elevation. These characteristics of the wave activity are similar to those of the depolarization wave reported in the chick embryo, suggesting that the large-scale depolarization wave is globally generated across different species.
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Hoffmann, Ulrike, Inna Sukhotinsky, Katharina Eikermann-Haerter, and Cenk Ayata. "Glucose Modulation of Spreading Depression Susceptibility." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (September 12, 2012): 191–95. http://dx.doi.org/10.1038/jcbfm.2012.132.
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Spreading depression of Leão is an intense spreading depolarization (SD) wave associated with massive transmembrane ionic, water, and neurotransmitter shifts. Spreading depolarization underlies migraine aura, and occurs in brain injury, making it a potential therapeutic target. While susceptibility to SD can be modulated pharmacologically, much less is known about modulation by systemic physiological factors, such as the glycemic state. In this study, we systematically examined modulation of SD susceptibility by blood glucose in anesthetized rats under full physiological monitoring. Hyperglycemia and hypoglycemia were induced by insulin or dextrose infusion (blood glucose ~40 and 400 mg/dL, respectively). Spreading depolarizations were evoked by direct cortical electrical stimulation to determine the intensity threshold, or by continuous topical KCl application to determine SD frequency. Hyperglycemia elevated the electrical SD threshold and reduced the frequency of KCl-induced SDs, without significantly affecting other SD properties. In contrast, hypoglycemia significantly prolonged individual and cumulative SD durations, but did not alter the electrical SD threshold, or SD frequency, amplitude or propagation speed. These data show that increased cerebral glucose availability makes the tissue resistant to SD.
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Smirnova, S. L., O. V. Suslonova, and I. M. Roshchevskaya. "Non-invasive detection of arrhythmogenic foci of atria by using the cardioelectric field on the surface of the body during experimental pulmonary hypertension." Jounal of arrhythmology 27, no. 1 (June 4, 2020): 63–69. http://dx.doi.org/10.35336/va-2020-1-63-69.
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Aim. The potential distribution of the cardioelectric field on the body surface during the initial atrial activity and the sequence of depolarization of the atrial subepicardium in rats with experimentally induced pulmonary hypertension were compared. This work is devoted to non-invasive detection of arrhythmogenic foci of atria by using the cardioelectric field on the body surface during experimental pulmonary hypertension.Materials and methods. The method of cardioelectrochronotopography has been used to study the electric field of the heart on the body surface and the sequence of propagation of the excitation wave along the atrial epicardium in rats with experimentally induced pulmonary hypertension caused by a single injection of monocrotaline (60 mg / kg, four weeks after drug administration).Results. Pulmonary hypertension causes the appearance of an additional focus of initial excitation in the area of the pulmonary vein lacunae, which leads to an increase in the heterogeneity of the propagation of the excitation wave along the atrial epicardium. The appearance of the additional excitation focus in the mouths of the pulmonary veins in the left atrium changes the picture of the sequence of depolarization of the atrial epicardium. The heterogeneity of the propagation of the excitation wave along the atrial epicardium is reflected in a different arrangement of zones of positive and negative cardioelectric potentials on the body surface before and during the P-wave in comparison with the initial state.Conclusion. Induced pulmonary hypertension contributes to the appearance of an additional focus of initial excitation in the area of the sleeves of the pulmonary veins of the left atrium in rats. This leads to an increase in the heterogeneity of the propagation of the excitation wave along the atrial epicardium. This is also reflected in the change in the arrangement of the zones of positive and negative cardioelectric potentials on the body surface before and during the P-wave in comparison with the initial state.
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Lopez, J. R., R. A. Ghanbari, and A. Terzic. "A KATP channel opener protects cardiomyocytes from Ca2+ waves: a laser confocal microscopy study." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (April 1, 1996): H1384—H1389. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1384.
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Laser confocal microscopy was used to visualize intracellular spatiotemporal Ca2+ patterns in single guinea pig ventricular myocytes loaded with the Ca2+ indicator, fluo 3-acetoxymethyl ester (fluo 3-AM), and exposed to moderately elevated extracellular K+ to induce partial membrane depolarization. Analysis of K(+)-induced intracellular Ca2+ elevation revealed three distinct paradigms: 1) diffuse, nonoscillatory Ca2+ elevation across the myocyte; 2) localized Ca2+ elevation in anatomically restricted areas (Ca2+ sparks); and 3) regenerative frontal propagations of Ca2+ that traversed the length of the cell (Ca2+ waves). The first two patterns were more frequently observed when the extracellular K+ concentration was raised to 8 mM. Ca2+ waves became more common when extracellular K+ concentration was increased to 16 mM, suggesting that a minimum threshold of increase in intracellular Ca2+ is necessary for the organization of Ca2+ waves. The velocity of propagation was typically approximately 60 microns/s with an average frequency of one wave per second crossing at a given point in the cell. Wave propagation resulted in spatial and temporal oscillations in cytosolic and nuclear Ca2+ concentration. Treating cardiac cells with aprikalim, a potassium channel-opening drug, prevented 16 mM K+ (but not 32 mM K+) from inducing an increase in Ca2+ concentration and from generating Ca2+ waves. In cardiomyocytes treated with glyburide, a selective antagonist of ATP-sensitive K+ channels, aprikalim failed to prevent 16 mM K+ from inducing Ca2+ waves. In summary, moderate hyperkalemia induces distinct nonuniform form patterns of intracellular Ca2+ elevation in ventricular cells, which can be prevented by a potassium channel-opening drug through a glyburide-sensitive mechanism.
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Csurgai-Horváth, László, Bernard Adjei-Frimpong, Carlo Riva, and Lorenzo Luini. "Radio Wave Satellite Propagation in Ka/Q Band." Periodica Polytechnica Electrical Engineering and Computer Science 62, no. 2 (May 23, 2018): 38–46. http://dx.doi.org/10.3311/ppee.11065.
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In 2013 the European Space Agency, in cooperation with Inmarsat, launched the Alphasat communication satellite hosting four Technology Demonstration Payloads (TDPs). One of them is the Aldo Paraboni payload, supported by the Italian Space Agency (ASI) and executed by ESA in the framework of the Advanced Research in Telecommunications Systems (ARTES) 8 Telecom program. In addition to the Communication experiment, it includes the Alphasat Scientific Experiment transmitting coherent beacon signals at Ka-band (19.701 GHz) and Q-band (39.402 GHz). The satellite supports a Europe-wide experiment to investigate the atmospheric propagation effects occurring in Ka and Q bands. The demand for increasing bandwidth in the satellite radio communication domain is moving the communication channels to the higher frequency bands. Hence for both research and commercial purposes is especially important to effectively explore the Q band that is affected by attenuation, depolarization and scintillation due to different atmospheric effects. In 2014 the Department of Broadband Infocommunications and Electromagnetic Theory at Budapest University of Technology and Economics joined the ASAPE (AlphaSat Aldo Paraboni Experimenters) group and developed a ground station to be installed in Budapest. This work was supported by the European Space Agency under its Plan for European Cooperating States program. Our paper gives the background of the Alphasat Scientific Experiment and overviews the design phases of the receiver station in Budapest. We present also the processing and validation of data recorded so far and our future experimenting plans.
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Boitier, Eric, Ruth Rea, and Michael R. Duchen. "Mitochondria Exert a Negative Feedback on the Propagation of Intracellular Ca2+ Waves in Rat Cortical Astrocytes." Journal of Cell Biology 145, no. 4 (May 17, 1999): 795–808. http://dx.doi.org/10.1083/jcb.145.4.795.
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We have used digital fluorescence imaging techniques to explore the interplay between mitochondrial Ca2+ uptake and physiological Ca2+ signaling in rat cortical astrocytes. A rise in cytosolic Ca2+ ([Ca2+]cyt), resulting from mobilization of ER Ca2+ stores was followed by a rise in mitochondrial Ca2+ ([Ca2+]m, monitored using rhod-2). Whereas [Ca2+]cyt recovered within ∼1 min, the time to recovery for [Ca2+]m was ∼30 min. Dissipating the mitochondrial membrane potential (Δψm, using the mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenyl-hydrazone [FCCP] with oligomycin) prevented mitochondrial Ca2+ uptake and slowed the rate of decay of [Ca2+]cyt transients, suggesting that mitochondrial Ca2+ uptake plays a significant role in the clearance of physiological [Ca2+]cyt loads in astrocytes. Ca2+ signals in these cells initiated either by receptor-mediated ER Ca2+ release or mechanical stimulation often consisted of propagating waves (measured using fluo-3). In response to either stimulus, the wave traveled at a mean speed of 22.9 ± 11.2 μm/s (n = 262). This was followed by a wave of mitochondrial depolarization (measured using tetramethylrhodamine ethyl ester [TMRE]), consistent with Ca2+ uptake into mitochondria as the Ca2+ wave traveled across the cell. Collapse of Δψm to prevent mitochondrial Ca2+ uptake significantly increased the rate of propagation of the Ca2+ waves by 50%. Taken together, these data suggest that cytosolic Ca2+ buffering by mitochondria provides a potent mechanism to regulate the localized spread of astrocytic Ca2+ signals.
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Kusters, J. M. A. M., W. P. M. van Meerwijk, D. L. Ypey, A. P. R. Theuvenet, and C. C. A. M. Gielen. "Fast calcium wave propagation mediated by electrically conducted excitation and boosted by CICR." American Journal of Physiology-Cell Physiology 294, no. 4 (April 2008): C917—C930. http://dx.doi.org/10.1152/ajpcell.00181.2007.
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We have investigated synchronization and propagation of calcium oscillations, mediated by gap junctional excitation transmission. For that purpose we used an experimentally based model of normal rat kidney (NRK) cells, electrically coupled in a one-dimensional configuration (linear strand). Fibroblasts such as NRK cells can form an excitable syncytium and generate spontaneous inositol 1,4,5-trisphosphate (IP3)-mediated intracellular calcium waves, which may spread over a monolayer culture in a coordinated fashion. An intracellular calcium oscillation in a pacemaker cell causes a membrane depolarization from within that cell via calcium-activated chloride channels, leading to an L-type calcium channel-based action potential (AP) in that cell. This AP is then transmitted to the electrically connected neighbor cell, and the calcium inflow during that transmitted AP triggers a calcium wave in that neighbor cell by opening of IP3 receptor channels, causing calcium-induced calcium release (CICR). In this way the calcium wave of the pacemaker cell is rapidly propagated by the electrically transmitted AP. Propagation of APs in a strand of cells depends on the number of terminal pacemaker cells, the L-type calcium conductance of the cells, and the electrical coupling between the cells. Our results show that the coupling between IP3-mediated calcium oscillations and AP firing provides a robust mechanism for fast propagation of activity across a network of cells, which is representative for many other cell types such as gastrointestinal cells, urethral cells, and pacemaker cells in the heart.
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Ma, Q., and A. Ishimaru. "Propagation and depolarization of an arbitrarily polarized wave obliquely incident on a slab of random medium." IEEE Transactions on Antennas and Propagation 39, no. 11 (1991): 1626–32. http://dx.doi.org/10.1109/8.102778.
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Williams, D. A., L. M. Delbridge, S. H. Cody, P. J. Harris, and T. O. Morgan. "Spontaneous and propagated calcium release in isolated cardiac myocytes viewed by confocal microscopy." American Journal of Physiology-Cell Physiology 262, no. 3 (March 1, 1992): C731—C742. http://dx.doi.org/10.1152/ajpcell.1992.262.3.c731.
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Laser scanning confocal microscopy of the Ca(2+)-sensitive fluorophore fluo-3 has been used to investigate spontaneous and propagated calcium release at high temporal and spatial resolution in enzymatically dispersed rat cardiomyocytes. Waves of fluorescence which propagated throughout the cytosol were evident in spontaneously contracting cardiac cells containing fluo-3, but not in cells containing Ca(2+)-insensitive fluorophores [2',7'-bis (carboxyethyl)-5,6-carboxyfluorescein, SNARF-1, rhodamine-123, or tetramethylrhodamine-labeled dextran]. These waves represent localized areas of elevated [Ca2+] [975 +/- 13 (SE) nM, range 800-1,500 nM; n = 16 cells]. Ca2+ waves were initiated by the spontaneous release of Ca2+ from the sarcoplasmic reticulum (SR) and propagated through cells at rates of 50-150 microns/s. Ca2+ waves were usually initiated at the cell ends, but multiple and variable initiation foci were observed in some cells. Where waves intersected within a single cell there was extinction of wave propagation, confirming the SR as the direct source of Ca2+ and revealing a refractory period in SR Ca2+ release. In some cells high-frequency Ca2+ waves lead to synchronized elevation of [Ca2+] throughout the entire cytosol and within the time period associated with cell depolarization. These observations support the hypothesis that some cardiac arrhythmias are initiated by spontaneous and propagated Ca2+ release and involve subsequent depolarization, global elevation of intracellular [Ca2+], and cell contraction.
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Zhou, Ning, Ravi L. Rungta, Aqsa Malik, Huili Han, Dong Chuan Wu, and Brian A. MacVicar. "Regenerative Glutamate Release by Presynaptic NMDA Receptors Contributes to Spreading Depression." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (July 3, 2013): 1582–94. http://dx.doi.org/10.1038/jcbfm.2013.113.
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Spreading depression (SD) is a slowly propagating neuronal depolarization that underlies certain neurologic conditions. The wave-like pattern of its propagation suggests that SD arises from an unusual form of neuronal communication. We used enzyme-based glutamate electrodes to show that during SD induced by transiently raising extracellular K+ concentrations ([K+]o) in rat brain slices, there was a rapid increase in the extracellular glutamate concentration that required vesicular exocytosis but unlike fast synaptic transmission, still occurred when voltage-gated sodium and calcium channels (VGSC and VGCC) were blocked. Instead, presynaptic N-methyl-D-aspartate (NMDA) receptors (NMDARs) were activated during SD and could generate substantial glutamate release to support regenerative glutamate release and propagating waves when VGSCs and VGCCs were blocked. In calcium-free solutions, high [K+]o still triggered SD-like waves and glutamate efflux. Under such a condition, glutamate release was blocked by mitochondrial Na+/Ca2+ exchanger inhibitors that likely blocked calcium release from mitochondria secondary to NMDA-induced Na+ influx. Therefore presynaptic NMDA receptor activation is sufficient for triggering vesicular glutamate release during SD via both calcium entry and release from mitochondria by mitochondrial Na+/Ca2+ exchanger. Our observations suggest that presynaptic NMDARs contribute to a cycle of glutamate-induced glutamate release that mediate high [K+]o-triggered SD.
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Joshi, I., and R. D. Andrew. "Imaging Anoxic Depolarization During Ischemia-Like Conditions in the Mouse Hemi-Brain Slice." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 414–24. http://dx.doi.org/10.1152/jn.2001.85.1.414.
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Focal ischemia evokes a sudden loss of membrane potential in neurons and glia of the ischemic core termed the anoxic depolarization (AD). In metabolically compromised regions with partial blood flow, peri-infarct depolarizations (PIDs) further drain energy reserves, promoting acute and delayed neuronal damage. Visualizing and quantifying the AD and PIDs and their acute deleterious effects are difficult in the intact animal. In the present study, we imaged intrinsic optical signals to measure changes in light transmittance in the mouse coronal hemi-brain slice during AD generation. The AD was induced by oxygen/glucose deprivation (OGD) or by ouabain exposure. Potential neuroprotective strategies using glutamate receptor antagonists or reduced temperature were tested. Eight minutes of OGD ( n = 18 slices) or 4 min of 100 μM ouabain ( n = 14) induced a focal increase of increased light transmittance (LT) in neocortical layers II/III that expanded concentrically to form a wave front coursing through neocortex and independently through striatum. The front was coincident with a negative voltage shift in extracellular potential. Wherever the LT front (denoting cell swelling) propagated, a decrease in LT (denoting dendritic beading) followed in its wake. In addition the evoked field potential was permanently lost, indicating neuronal damage. Glutamate receptor antagonists did not block the onset and propagation of AD or the extent of irreversible damage post-AD. Lowering temperature to 25–30°C protected the tissue from OGD damage by inhibiting AD onset. This study shows that anoxic depolarization evoked by global ischemia-like conditions is a spreading process that is focally initiated at multiple sites in cortical and subcortical gray. The combined energy demands of O2/glucose deprivation and the AD greatly exacerbate neuronal damage. Glutamate receptor antagonists neither block the AD in the ischemic core nor, we propose, block recurrent PID arising close to the core.
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Lin, Joyce W., Libet Garber, Yue Rosa Qi, Marvin G. Chang, Joshua Cysyk, and Leslie Tung. "Region of slowed conduction acts as core for spiral wave reentry in cardiac cell monolayers." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (January 2008): H58—H65. http://dx.doi.org/10.1152/ajpheart.00631.2007.
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Pathophysiological heterogeneity in cardiac tissue is related to the occurrence of arrhythmias. Of importance are regions of slowed conduction, which have been implicated in the formation of conduction block and reentry. Experimentally, it has been a challenge to produce local heterogeneity in a manner that is both reversible and well controlled. Consequently, we developed a dual-zone superfusion chamber that can dynamically create a small (5 mm) central island of heterogeneity in cultured cardiac cell monolayers. Three different conditions were studied to explore the effect of regionally slowed conduction on wave propagation and reentry: depolarization by elevated extracellular potassium, sodium channel inhibition with lidocaine, and cell-cell decoupling with palmitoleic acid. Using optical mapping of transmembrane voltage, we found that the central region of slowed conduction always served as the core region around which a spiral wave formed and then revolved following a period of rapid pacing. Because of the localized slowing in the core region, we observed experimentally for the first time an S shape of the spiral wave front near its tip. These results indicate that a small region of slowed conduction can play a crucial role in the formation, anchoring, and modulation of reentrant spiral waves.
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Bardakjian, B. L., and E. J. Vigmond. "Effects of the propagation velocity of a surface depolarization wave on the extracellular potential of an excitable cell." IEEE Transactions on Biomedical Engineering 41, no. 5 (May 1994): 432–39. http://dx.doi.org/10.1109/10.293217.
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Xu, Weifeng, Brian S. Wolff, and Jian-young Wu. "Low-intensity electric fields induce two distinct response components in neocortical neuronal populations." Journal of Neurophysiology 112, no. 10 (November 15, 2014): 2446–56. http://dx.doi.org/10.1152/jn.00740.2013.
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Low-intensity alternating electric fields applied to the scalp are capable of modulating cortical activity and brain functions, but the underlying mechanisms remain largely unknown. Here, we report two distinct components of voltage-sensitive dye signals induced by low-intensity, alternating electric fields in rodent cortical slices: a “passive component,” which corresponds to membrane potential changes directly induced by the electric field; and an “active component,” which is a widespread depolarization that is dependent on excitatory synaptic transmission. The passive component is stationary, with amplitude and phase accurately reflecting the cortical cytoarchitecture. In contrast, the active component is initiated from a local “hot spot” of activity and spreads to a large population as a propagating wave with rich local dynamics. The propagation of the active component may play a role in modulating large-scale cortical activity by spreading a low level of excitation from a small initiation point to a vast neuronal population.
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Terasaka, D., A. Bortoff, and L. F. Sillin. "Postprandial changes in intestinal slow-wave propagation reflect a decrease in cell coupling." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 3 (September 1, 1989): G463—G469. http://dx.doi.org/10.1152/ajpgi.1989.257.3.g463.
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The purpose of these studies was to determine the effects of feeding on jejunal slow-wave propagation velocity (SWPV). Nine cats were instrumented with six pairs of electrodes implanted 4 cm apart on the jejunum. Electrical activity was recorded at the end of an 18-h fast after which each animal was fed 60 g of canned cat food. Recordings were continued during feeding and for several hours thereafter. This procedure was repeated at least twice for each cat. Average SWPV (cm/s) decreased from a fasting level of 2.28 +/- 0.20 (mean of means +/- SE) to 1.93 +/- 0.16 at 10-20 min, 1.51 +/- 0.11 at 1 h, and 1.37 +/- 0.10 at 3 h postprandially. Corresponding SW frequencies (SWFs) were 19.6 +/- 0.3, 18.7 +/- 0.2, 19.2 +/- 0.2, and 19.0 +/- 0.2 cycles/min, respectively. The differences between the fasting SWPV and that at 1 and 3 h were significant (P less than 0.05). When SWPV was plotted as a function of SWF, the slopes of the corresponding curves were also found to decrease postprandially (P less than 0.05, fasting vs. 1 and 3 h). There was no apparent change in SW amplitude, maximum rate of SW depolarization, or threshold. In the absence of changes in these parameters, the divergence of the slopes at lower SWFs indicates that the decrease in SWPV is because of increased internal resistance, probably the result of uncoupling of intestinal muscle cells. The change is rapid in onset and long in duration, suggesting that an uncoupling factor is released during ingestion of a meal, and that its effect persists for several hours.
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Aitken, P. G., G. C. Tombaugh, D. A. Turner, and G. G. Somjen. "Similar Propagation of SD and Hypoxic SD-Like Depolarization in Rat Hippocampus Recorded Optically and Electrically." Journal of Neurophysiology 80, no. 3 (September 1, 1998): 1514–21. http://dx.doi.org/10.1152/jn.1998.80.3.1514.
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Aitken, P. G., G. C. Tombaugh, D. A. Turner, and G. G. Somjen. Similar propagation of SD and hypoxic SD-like depolarization in rat hippocampus recorded optically and electrically. J. Neurophysiol. 80: 1514–1521, 1998. Neuron membrane changes and ion redistribution during normoxic spreading depression (SD) induced, for example, by potassium injection, closely resemble those that occur during hypoxic SD-like depolarization (HSD) induced by oxygen withdrawal, but the degree to which the two phenomena are related is controversial. We used extracellular electrical recording and imaging of intrinsic optical signals in hippocampal tissue slices to compare 1) initiation and spread of these two phenomena and 2) the effects of putative gap junction blocking agents, heptanol and octanol. Both events arose focally, after which a clear advancing wave front of increased reflectance and DC shift spread along the CA1 stratum radiatum and s. oriens. The rate of spread was similar: conduction velocity of normoxic SD was 8.73 ± 0.92 mm/min (mean ± SE) measured electrically and 5.84 ± 0.63 mm/min measured optically, whereas HSD showed values of 7.22 ± 1.60 mm/min (electrical) and 6.79 ± 0.42 mm/min (optical). When initiated in CA1, normoxic SD consistently failed to enter the CA3 region (7/7 slices) and could not be initiated by direct KCl injection in the CA3 region ( n = 3). Likewise, the hypoxic SD-like optical signal showed onset in the CA1 region and halted at the CA1/CA3 boundary (9/9 slices), but in some (4/9) slices the dentate gyrus region showed a separate onset of signal changes. Microinjection into CA1 stratum radiatum of octanol (1 mM), which when bath applied arrests the spread of normoxic SD, created a small focus that appeared to be protected from hypoxic depolarization. However, bath application of heptanol (3 mM) or octanol (2 mM) did not prevent the spread of HSD, although the onset was delayed. This suggests that, although gap junctions may be essential for the spread of normoxic SD, they may play a less important role in the spread of HSD.
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Woo, Sun-Hee, Seon-Hwa Hwang, Joon-Chul Kim, and Martin Morad. "Enhancement of Ca2+Current Does Not Regulate the Speed of Depolarization-induced Ca2+Propagation Wave in Rat Atrial Myocytes." Biomolecules and Therapeutics 15, no. 4 (December 31, 2007): 212–17. http://dx.doi.org/10.4062/biomolther.2007.15.4.212.
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Amzica, Florin, and Dag Neckelmann. "Membrane Capacitance of Cortical Neurons and Glia During Sleep Oscillations and Spike-Wave Seizures." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2731–46. http://dx.doi.org/10.1152/jn.1999.82.5.2731.
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Dual intracellular recordings in vivo were used to disclose relationships between cortical neurons and glia during spontaneous slow (<1 Hz) sleep oscillations and spike-wave (SW) seizures in cat. Glial cells displayed a slow membrane potential oscillation (<1 Hz), in close synchrony with cortical neurons. In glia, each cycle of this oscillation was made of a round depolarizing potential of 1.5–3 mV. The depolarizing slope corresponded to a steady depolarization and sustained synaptic activity in neurons (duration, 0.5–0.8 s). The repolarization of the glial membrane (duration, 0.5–0.8 s) coincided with neuronal hyperpolarization, associated with disfacilitation, and suppressed synaptic activity in cortical networks. SW seizures in glial cells displayed phasic events, synchronized with neuronal paroxysmal potentials, superimposed on a plateau of depolarization, that lasted for the duration of the seizure. Measurements of the neuronal membrane capacitance during slow oscillating patterns showed small fluctuations around the resting values in relation to the phases of the slow oscillation. In contrast, the glial capacitance displayed a small-amplitude oscillation of 1–2 Hz, independent of phasic sleep and seizure activity. Additionally, in both cell types, SW seizures were associated with a modulatory, slower oscillation (≈0.2 Hz) and a persistent increase of capacitance, developing in parallel with the progression of the seizure. These capacitance variations were dependent on the severity of the seizure and the distance between the presumed seizure focus and the recording site. We suggest that the capacitance variations may reflect changes in the membrane surface area (swelling) and/or of the interglial communication via gap junctions, which may affect the synchronization and propagation of paroxysmal activities.
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Fujita, Shuji, Hideo Maeno, and Kenichi Matsuoka. "Radio-wave depolarization and scattering within ice sheets: a matrix-based model to link radar and ice-core measurements and its application." Journal of Glaciology 52, no. 178 (2006): 407–24. http://dx.doi.org/10.3189/172756506781828548.
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AbstractCrystal-orientation fabric (COF) has a large influence on ice-sheet flow. Earlier radar studies have shown that COF-based birefringence occurs within ice sheets. Radio-wave scattering in polar ice results from changing physical properties of permittivity and conductivity that arise from differing values of density, acidity and COF. We present an improved mathematical model that can handle all these phenomena together. We use this matrix-based model to study the two-way propagation of depolarized radio waves that scatter at both isotropic and anisotropic boundaries. Based on numerical simulations, we demonstrate how COF affects the radar signals in terms of radar polarization and frequency. We then compare the simulated features with VHF radar data obtained at two contrasting inland sites in East Antarctica, where COF is known from ice-core studies. These two sites are Dome Fuji, located near a dome summit, and Mizuho, located in a converging ice-flow region. Data at Dome Fuji are dominated by typical features resulting from birefringence. In contrast, both birefringence and anisotropic scattering affect the radar data at Mizuho. We argue that radar methods can be used to determine principal axes and strength of birefringence in the ice sheets.
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Zheng, Haifeng, Kyung Sik Park, Sang Don Koh, and Kenton M. Sanders. "Expression and function of a T-type Ca2+ conductance in interstitial cells of Cajal of the murine small intestine." American Journal of Physiology-Cell Physiology 306, no. 7 (April 1, 2014): C705—C713. http://dx.doi.org/10.1152/ajpcell.00390.2013.
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Interstitial cells of Cajal (ICC) generate slow waves in gastrointestinal (GI) muscles. Previous studies have suggested that slow wave generation and propagation depends on a voltage-dependent Ca2+ entry mechanism with the signature of a T-type Ca2+ conductance. We studied voltage-dependent inward currents in isolated ICC. ICC displayed two phases of inward current upon depolarization: a low voltage-activated inward current and a high voltage-activated current. The latter was of smaller current density and blocked by nicardipine. Ni2+ (30 μM) or mibefradil (1 μM) blocked the low voltage-activated current. Replacement of extracellular Ca2+ with Ba2+ did not affect the current, suggesting that either charge carrier was equally permeable. Half-activation and half-inactivation occurred at −36 and −59 mV, respectively. Temperature sensitivity of the Ca2+ current was also characterized. Increasing temperature (20–30°C) augmented peak current from −7 to −19 pA and decreased the activation time from 20.6 to 7.5 ms [temperature coefficient (Q10) = 3.0]. Molecular studies showed expression of Cacna1g (Cav3.1) and Cacna1h (Cav3.2) in ICC. The temperature dependence of slow waves in intact jejunal muscles of wild-type and Cacna1h −/− mice was tested. Reducing temperature decreased the upstroke velocity significantly. Upstroke velocity was also reduced in muscles of Cacna1h −/− mice, and Ni2+ or reduced temperature had little effect on these muscles. Our data show that a T-type conductance is expressed and functional in ICC. With previous studies our data suggest that T-type current is required for entrainment of pacemaker activity within ICC and for active propagation of slow waves in ICC networks.
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Bringi and Zrnic. "Polarization Weather Radar Development from 1970–1995: Personal Reflections." Atmosphere 10, no. 11 (November 15, 2019): 714. http://dx.doi.org/10.3390/atmos10110714.
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The modern era of polarimetric radar begins with radiowave propagation research starting in the early 1970s with applications to measurement and modeling of wave attenuation in rain and depolarization due to ice particles along satellite–earth links. While there is a rich history of radar in meteorology after World War II, the impetus provided by radiowave propagation requirements led to high-quality antennas and feeds. Our journey starts by describing the key institutions and personnel responsible for development of weather radar polarimetry. The early period was dominated by circularly polarized radars for propagation research and at S band (frequency near 3 GHz) for hail detection. By the mid to late 70s, a paradigm shift occurred which led to the dominance of linear polarizations with applications to slant path attenuation prediction as well as estimation of rain rates and inferences of precipitation physics. The period from the early 1980s to 1995 can be considered as the “golden” period of rapid research that brought in meteorologists, cloud physicists, and hydrologists. This article describes the evolution of this technology from the vantage point of the authors. Their personal reflections and “behind the scenes” descriptions offer a glimpse into the inner workings at several key institutions which cannot be found elsewhere.
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SUN, XIAOLI, PENGCHENG LI, WEIHUA LUO, BIYING GONG, and QINGMING LUO. "ACCURATELY DETERMINING PROPAGATION VELOCITY OF CORTICAL SPREADING DEPRESSION IN RATS BY OPTICAL INTRINSIC SIGNAL IMAGING." Journal of Innovative Optical Health Sciences 03, no. 02 (April 2010): 103–8. http://dx.doi.org/10.1142/s1793545810000915.
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Cortical spreading depression (CSD) is a wave of neuronal and glial depolarization that propagates across the cortex at a rate of 2–5 mm/min accompanied by reversible electroencephalogram (EEG) suppression, a negative shift of direct current (DC) potential, and change of optical intrinsic signals (OIS). Propagation velocity of CSD is an important parameter used to study this phenomenon. It is commonly determined in an electrophysiological way that measures the time required for a CSD wave to pass along two electrodes. Since the electrophysiology technique fails to reveal the spreading pattern of CSD, velocity calculated in this manner might be inaccurate. In this study, we combined the electrophysiological recording and OIS imaging (OISI) for detecting changes in DC potential and OIS during CSD simultaneously. An optical method based on OISI to determine the CSD velocity, which is measured by generating a series of regions of interest (ROI) perpendicular to the advancing wavefront along propagation direction of CSD at different time points and then dividing by the distance between ROIs over time, is presented. Comparison of the accuracy of the two approaches in determining the CSD velocity is made as well. The average rate of 33 CSDs is 3.52 ± 0.87 mm/min by use of the optical method and 4.36 ± 1.65 mm/min by use of the electrophysiological method. Because of the information about spreading pattern of CSD provided optically, the velocity determined by OISI is of smaller deviation and higher accuracy.
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Momose-Sato, Yoko, Tomoharu Nakamori, and Katsushige Sato. "Spontaneous depolarization wave in the mouse embryo: origin and large-scale propagation over the CNS identified with voltage-sensitive dye imaging." European Journal of Neuroscience 35, no. 8 (February 17, 2012): 1230–41. http://dx.doi.org/10.1111/j.1460-9568.2012.07997.x.
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Alvarez, J. M., M. A. Vaughan, C. A. Hostetler, W. H. Hunt, and D. M. Winker. "Calibration Technique for Polarization-Sensitive Lidars." Journal of Atmospheric and Oceanic Technology 23, no. 5 (May 1, 2006): 683–99. http://dx.doi.org/10.1175/jtech1872.1.
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Abstract Polarization-sensitive lidars have proven to be highly effective in discriminating between spherical and nonspherical particles in the atmosphere. These lidars use a linearly polarized laser and are equipped with a receiver that can separately measure the components of the return signal polarized parallel and perpendicular to the outgoing beam. In this work a technique for calibrating polarization-sensitive lidars is described that was originally developed at NASA's Langley Research Center (LaRC) and has been used continually over the past 15 yr. The procedure uses a rotatable half-wave plate inserted into the optical path of the lidar receiver to introduce controlled amounts of polarization cross talk into a sequence of atmospheric backscatter measurements. Solving the resulting system of nonlinear equations generates the system calibration constants (gain ratio and offset angle) required for deriving calibrated measurements of depolarization ratio from the lidar signals. In addition, this procedure also determines the mean depolarization ratio within the region of the atmosphere that is analyzed. Simulations and error propagation studies show the method to be both reliable and well behaved. Operational details of the technique are illustrated using measurements obtained as part of LaRC's participation in the First International Satellite Cloud Climatology Project Regional Experiment.
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Toda, S., S. Kawahara, and Y. Kirino. "Image analysis of olfactory responses in the procerebrum of the terrestrial slug Limax marginatus." Journal of Experimental Biology 203, no. 19 (October 1, 2000): 2895–905. http://dx.doi.org/10.1242/jeb.203.19.2895.
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Neural oscillations have been found to occur in the olfactory centers of some vertebrates and invertebrates, including the procerebrum of the terrestrial slug Limax marginatus. Using optical recording with the potential-sensitive dye di-4-ANEPPS, we analyzed the spatiotemporal pattern of procerebral neural activities in response to odorants applied to an in vitro brain-superior tentacle preparation. The odor of rat chow, on which the slugs were normally fed, increased the frequency of the oscillation. Garlic odor, which induced aversive behavior in the slug, caused a transient increase in oscillation frequency during stimulation, followed by a second increase in oscillation frequency when the stimulus was terminated. Wave propagation from the distal to the proximal region of the procerebrum was accelerated in parallel with modulation of the frequency. The cycle-by-cycle average of the optical signals showed that a large area of the cerebral ganglia, including the procerebrum, was depolarized during the initial increase in frequency. During the second increase, however, the net depolarization was most prominent in the terminal mass of the procerebrum. These results suggest that the level of depolarization generated by interactions among the neurites projecting to the terminal mass, such as the neurites of the nonbursting neurons, may control neural oscillations in the procerebrum.
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Nagel, Claudia, Nicolas Pilia, Laura Unger, and Olaf Dössel. "Performance of Different Atrial Conduction Velocity Estimation Algorithms Improves with Knowledge about the Depolarization Pattern." Current Directions in Biomedical Engineering 5, no. 1 (September 1, 2019): 101–4. http://dx.doi.org/10.1515/cdbme-2019-0026.
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AbstractQuantifying the atrial conduction velocity (CV) reveals important information for targeting critical arrhythmia sites that initiate and sustain abnormal electrical pathways, e.g. during atrial flutter. The knowledge about the local CV distribution on the atrial surface thus enhances clinical catheter ablation procedures by localizing pathological propagation paths to be eliminated during the intervention. Several algorithms have been proposed for estimating the CV. All of them are solely based on the local activation times calculated from electroanatomical mapping data. They deliver false values for the CV if applied to regions near scars or wave collisions. We propose an extension to all approaches by including a distinct preprocessing step. Thereby, we first identify scars and wave front collisions and provide this information for the CV estimation algorithm. In addition, we provide reliable CV values even in the presence of noise. We compared the performance of the Triangulation, the Polynomial Fit and the Radial Basis Functions approach with and without the inclusion of the aforementioned preprocessing step. The evaluation was based on different activation patterns simulated on a 2D synthetic triangular mesh with different levels of noise added. The results of this study demonstrate that the accuracy of the estimated CV does improve when knowledge about the depolarization pattern is included. Over all investigated test cases, the reduction of the mean velocity error quantified to at least 25 mm/s for the Radial Basis Functions, 14 mm/s for the Polynomial Fit and 14 mm/s for the Triangulation approach compared to their respective implementations without the preprocessing step. Given the present results, this novel approach can contribute to a more accurate and reliable CV estimation in a clinical setting and thus improve the success of radio-frequency ablation to treat cardiac arrhythmias.
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XU, TINGTING, PENGCHENG LI, SHANGBIN CHEN, and WEIHUA LUO. "TWO-DIMENSIONAL VISUALIZATION OF THE PROPAGATION SPEED OF CORTICAL SPREADING DEPRESSION IN RAT CORTEX." Journal of Innovative Optical Health Sciences 03, no. 01 (January 2010): 75–80. http://dx.doi.org/10.1142/s1793545810000873.
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Cortical spreading depression (CSD), which is a significant pathological phenomenon that correlates with migraines and cerebral ischemia, has been characterized by a wave of depolarization among neuronal cells and propagates across the cortex at a rate of 2–5 mm/min. Although the propagation pattern of CSD was well-investigated using high-resolution optical imaging technique, the variation of propagation speed of CSD across different regions of cortex was not well-concerned, partially because of the lack of ideal approach to visualize two-dimensional distribution of propagation speed of CSD over the whole imaged cortex. Here, we have presented a method to compute automatically the propagation speed of CSD throughout every spots in the imaged cortex. In this method, temporal clustering analysis (TCA) and least square estimation (LSE) were first used to detect origin site where CSD was induced. Taking the origin site of CSD as the origin of coordinates, the data matrix of each image was transformed into the corresponding points based on the polar-coordinate representation. Then, two fixed-distance regions of interest (ROIs) are sliding along with the radial coordinate at each polar angle within the image for calculating the time lag with correlating algorithm. Finally, we could draw a two-dimensional image, in which the value of each pixel represented the velocity of CSD when it spread through the corresponding area of the imaged cortex. The results demonstrated that the method can reveal the heterogeneity of propagation speed of CSD in the imaged cortex with high fidelity and intuition.
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Yussuff, Abayomi Isiaka, and Nor Hisham Haji Khamis. "Rain Attenuation Prediction Model for Lagos at Millimeter Wave Bands." Journal of Atmospheric and Oceanic Technology 31, no. 3 (March 1, 2014): 639–46. http://dx.doi.org/10.1175/jtech-d-13-00024.1.
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Abstract Lagos, Nigeria (6.35°N, 3.2°E), is a coastal station in the rain forest area of southwestern Nigeria with an altitude of 38 m. Since most communication now takes place above the X band because of congestion of lower bands, it was necessary to look into ways of maximizing X-band usage. There are inadequate data for use in rain propagation studies at microwave frequencies, and even less so at millimeter wave bands where most of the signal depolarization and fading has been discovered to exist. The proposed model is a modification of the International Telecommunication Union–Radio Communication Sector (ITU-R) model combined with locally obtained regression coefficients for estimating specific attenuation as proposed by G. Olalere Ajayi. The Dissanayake, Allnutt, and Haidara (DAH), Simple Attenuation Model (SAM), and ITU-R attenuation prediction models were investigated along with the proposed model. The ITU-R model was observed to produce the best results at 40 GHz, with percentage error values of 0.61%, 0.55%, and 0.49% at 0.1%, 0.01%, and 0.001% of the time, respectively. In comparison, the proposed prediction model showed good performance at 20-GHz down-link frequency, with percentage error values of 3.6%, 3.3%, and 2.9% at 0.1%, 0.01%, and 0.001% of the time, respectively. The obtained results also showed good agreement with other similar works in the open literature. The results presented in this work are valuable for the design and planning of a satellite link in the tropical regions.
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Autio, Joonas A., Artem Shatillo, Rashid Giniatullin, and Olli H. Gröhn. "Parenchymal Spin-Lock fMRI Signals Associated with Cortical Spreading Depression." Journal of Cerebral Blood Flow & Metabolism 34, no. 5 (February 5, 2014): 768–75. http://dx.doi.org/10.1038/jcbfm.2014.16.
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We found novel types of parenchymal functional magnetic resonance imaging (fMRI) signals in the rat brain during large increases in metabolism. Cortical spreading depression (CSD), a self-propagating wave of cellular activation, is associated with several pathologic conditions such as migraine and stroke. It was used as a paradigm to evoke transient neuronal depolarization leading to enhanced energy consumption. Activation of CSD was investigated using spin-lock (SL), diffusion, blood oxygenation level-dependent and cerebral blood volume fMRI techniques. Our results show that the SL-fMRI signal is generated by endogenous parenchymal mechanisms during CSD propagation, and these mechanisms are not associated with hemodynamic changes or cellular swelling. Protein phantoms suggest that pH change alone does not explain the observed SL-fMRI signal changes. However, increased amounts of inorganic phosphates released from high-energy phosphates combined with pH changes may produce SL- power-dependent longitudinal relaxation in the rotating frame ( R1ρ) changes in protein phantoms that are similar to those observed during CSD, as seen before in acute ischemia under our experimental conditions. This links SL-fMRI changes intimately to energy metabolism and supports the use of the SL technique as a new, promising functional approach for noninvasive imaging of metabolic transitions in the active or pathologic brain.
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Bian, Nannan, Yi Yuan, Yingwei Li, Mengyang Liu, and Xiaoli Li. "Low-Intensity Pulsed Ultrasound Stimulation Inhibits Cortical Spreading Depression." Cerebral Cortex 31, no. 8 (April 15, 2021): 3872–80. http://dx.doi.org/10.1093/cercor/bhab055.
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Abstract Cortical spreading depression (CSD), which is closely correlated with migraine aura, cerebral ischemia, seizure, and brain injury, is a spreading wave of neuronal and glial depolarization. The purpose of this study is to investigate whether low-intensity pulsed ultrasound stimulation (PUS) inhibits CSD by modulating neural activity and hemodynamics. Behavioral test, intrinsic signal optical imaging and western blot analysis were used for evaluating the inhibition effect of PUS on CSD in rat. We found that: 1) 30 min of PUS can significantly improve motor activity of rat with CSD. 2) Both 30 s and 30 min of PUS can significantly reduce count and propagation speed of CSD in rat and the inhibitory effect was enhanced with increase of ultrasound intensity. 3) 30 min of PUS significantly enhanced levels of brain-derived neurotrophic factor protein in brain tissue with CSD. These results suggest that PUS has the potential to treat brain disorders associated with CSD.
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Kastrup, Andreas, Tobias Neumann-Haefelin, Michael E. Moseley, and Alex de Crespigny. "High Speed Diffusion Magnetic Resonance Imaging of Ischemia and Spontaneous Periinfarct Spreading Depression after Thromboembolic Stroke in the Rat." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1636–47. http://dx.doi.org/10.1097/00004647-200012000-00003.
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Spontaneous episodes of transient cell membrane depolarization (spreading depression [SD]) occur in the surroundings of experimental stroke lesions and are believed to contribute to infarct growth. Diffusion-weighted imaging (DWI) is capable of detecting the water shifts from extracellular to intracellular space associated with SD waves and ischemia, and can make in vivo measurements of these two features on a pixel-by-pixel basis with good temporal resolution. Using continuous high speed DWI with a temporal resolution of 12 seconds over a period of 3 hours, the in vivo contribution of spontaneous SDs to the development of ischemic tissue injury was examined in 8 rats using a thromboembolic stroke model. During the observation period, the initial lesion volume increased in 4 animals, remained unchanged in 1 animal, and decreased in 3 animals (most likely because of spontaneous clot lysis). Irrespective of the lesion evolution patterns, animals demonstrated 6.5 ± 2.1 spontaneous SDs outside of the ischemic core. A time-to-peak analysis of apparent diffusion coefficient (ADC) changes for each SD wave demonstrated multidirectional propagation patterns from variable initiation sites. Maps of the time constants of ADC recovery, reflecting the local energy supply and cerebral blood flow, revealed prolonged recovery times in areas close to the ischemic core. However, repetitive SD episodes in the periinfarct tissue did not eventually lead to permanent ADC reductions. These results suggest that spontaneous SD waves do not necessarily contribute to the expansion of the ischemic lesion volume in this model.
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Balse, Elise, David F. Steele, Hugues Abriel, Alain Coulombe, David Fedida, and Stéphane N. Hatem. "Dynamic of Ion Channel Expression at the Plasma Membrane of Cardiomyocytes." Physiological Reviews 92, no. 3 (July 2012): 1317–58. http://dx.doi.org/10.1152/physrev.00041.2011.
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Cardiac myocytes are characterized by distinct structural and functional entities involved in the generation and transmission of the action potential and the excitation-contraction coupling process. Key to their function is the specific organization of ion channels and transporters to and within distinct membrane domains, which supports the anisotropic propagation of the depolarization wave. This review addresses the current knowledge on the molecular actors regulating the distinct trafficking and targeting mechanisms of ion channels in the highly polarized cardiac myocyte. In addition to ubiquitous mechanisms shared by other excitable cells, cardiac myocytes show unique specialization, illustrated by the molecular organization of myocyte-myocyte contacts, e.g., the intercalated disc and the gap junction. Many factors contribute to the specialization of the cardiac sarcolemma and the functional expression of cardiac ion channels, including various anchoring proteins, motors, small GTPases, membrane lipids, and cholesterol. The discovery of genetic defects in some of these actors, leading to complex cardiac disorders, emphasizes the importance of trafficking and targeting of ion channels to cardiac function. A major challenge in the field is to understand how these and other actors work together in intact myocytes to fine-tune ion channel expression and control cardiac excitability.
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Alexander, Bryce, Gary Tse, Manuel Martinez-Selles, and Adrian Baranchuk. "Atrial Conduction Disorders." Current Cardiology Reviews 17, no. 1 (March 11, 2021): 68–73. http://dx.doi.org/10.2174/1573403x17666210112161524.
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Atrial conduction disorders result from impaired propagation of cardiac impulses from the sinoatrial node through the atrial conduction pathways. Disorders affecting interatrial conduction alter P-wave characteristics on the surface electrocardiogram. A variety of P-wave indices reflecting derangements in atrial conduction have been described and have been associated with an increased risk of atrial fibrillation (AF) and stroke. Interatrial block (IAB) is the most well-known of the different P-wave indices and is important clinically due to its ability to predict patients who are at risk of the development of AF and other supraventricular tachycardias. P-Wave Axis is a measure of the net direction of atrial depolarization and is determined by calculating the net vector of the P-wave electrical activation in the six limb-leads using the hexaxial reference system. It has been associated with stroke and it has been proposed that this variable be added to the existing CHA2DS2-VASc score to create a P2-CHA2DS2-VASc score to improve stroke prediction. P-Terminal Force in V1 is thought to be an epiphenomenon of advanced atrial fibrotic disease and has been shown to be associated with a higher risk of death, cardiac death, and congestive heart failure as well as an increased risk of AF. P-wave Dispersion is defined as the difference between the shortest and longest P-wave duration recorded on multiple concurrent surface ECG leads on a standard 12-lead ECG and has also been associated with the development of AF and AF recurrence. Pwave voltage in lead I (PVL1) is thought to be an electrocardiographic representation of cardiac conductive properties and, therefore, the extent of atrial fibrosis relative to myocardial mass. Reduced PVL1 has been demonstrated to be associated with new-onset AF in patients with coronary artery disease and may be useful for predicting AF. Recently a risk score (the MVP risk score) has been developed using IAB and PVL1 to predict atrial fibrillation and has shown a good predictive ability to determine patients at high risk of developing atrial fibrillation. The MVP risk score is currently undergoing validation in other populations. This section reviews the different P-wave indices in-depth, reflecting atrial conduction abnormalities.
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Castelnovo, Anna, Cecilia Casetta, Francesco Donati, Renata del Giudice, Caroline Zangani, Simone Sarasso, and Armando D’Agostino. "S6. SLEEP ENDOPHENOTYPES OF SCHIZOPHRENIA: A HIGH-DENSITY EEG STUDY IN DRUG-NAïVE, FIRST EPISODE PSYCHOSIS PATIENTS." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S32. http://dx.doi.org/10.1093/schbul/sbaa031.072.
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Abstract Background Slow waves, the hallmark of the deep nonrapid eye movement sleep electroencephalogram (EEG), are critical for restorative sleep and brain plasticity. They arise from the synchronous depolarization and hyperpolarization of millions of cortical neurons and their proper generation and propagation relies upon the integrity of widespread cortico-thalamic networks. Slow wave abnormalities have been reported in patient with Schizophrenia, although with partially contradictory results, probably related to antipsychotic and sedative medications. Recently, their presence and delineation, have been convincingly shown in first-episode psychosis patients (FEP). However, clear evidence of this biomarker at the onset of the disease, prior to any psychopharmacological intervention, remains limited. Moreover, no attempt has been made to elucidate the prognostic meaning of this finding. Methods We collected whole night sleep high–density electroencephalography recordings (64-channel BrainAmp, Brain Products GmbH, Gilching, Germany) in 20 drug-naive FEP patients and 20 healthy control subjects (HC). Several clinical psychometric scales as well as neurocognitive tests were administered to all subjects in order to better define psychopathological status and vulnerability. EEG slow wave activity (SWA, spectral power between 1 and 4 Hz) and several slow wave parameters were computed at each electrode location, including density and amplitude, at each electrode location. Along with a group analysis between FEP and HC, a subgroup analysis was also computed between patients who showed a progression of symptoms to full-blown Schizophrenia (SCZ, n = 10) over the next 12-month follow-up and those who did not (OTH, n = 10). Results Sleep macro-architecture was globally preserved in FEP patients. SWA (1–4 Hz) was lower in FEP compared to HC but this difference didn’t reach statistical significance. Slow wave density was decreased in FEP compared to HC, with a significance that survived multiple comparison correction over a large fronto-central cluster. Mean amplitude was preserved. At the subgroup analysis, these results were largely driven by the subgroup of patients with a confirmed diagnosis of SCZ at a 12-month follow-up. Indeed, no difference could be found between OTH and HC, while a strong significance was still evident between SCZ and HC. Discussion Our data confirm previous findings on reduced slow wave density in FEP, and expand them to acute subjects, before any treatment is prescribed. This is in line with available data on diffuse abnormalities of cortico-cortical and cortico-thalamic networks in these patients. Interestingly, our data also offer preliminary evidence that this deficit is specific for SCZ, as it appears to differentiate patients who developed SCZ from those with other diagnoses at follow-up. Given the traveling properties of slow waves, future research should establish their potential as markers of connectivity in SCZ.
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Firl, Alana, Georgeann S. Sack, Zachary L. Newman, Hiroaki Tani, and Marla B. Feller. "Extrasynaptic glutamate and inhibitory neurotransmission modulate ganglion cell participation during glutamatergic retinal waves." Journal of Neurophysiology 109, no. 7 (April 1, 2013): 1969–78. http://dx.doi.org/10.1152/jn.00039.2013.
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During the first 2 wk of mouse postnatal development, transient retinal circuits give rise to the spontaneous initiation and lateral propagation of depolarizations across the ganglion cell layer (GCL). Glutamatergic retinal waves occur during the second postnatal week, when GCL depolarizations are mediated by ionotropic glutamate receptors. Bipolar cells are the primary source of glutamate in the inner retina, indicating that the propagation of waves depends on their activation. Using the fluorescence resonance energy transfer-based optical sensor of glutamate FLII81E-1μ, we found that retinal waves are accompanied by a large transient increase in extrasynaptic glutamate throughout the inner plexiform layer. Using two-photon Ca2+ imaging to record spontaneous Ca2+ transients in large populations of cells, we found that despite this spatially diffuse source of depolarization, only a subset of neurons in the GCL and inner nuclear layer (INL) are robustly depolarized during retinal waves. Application of the glutamate transporter blocker dl-threo-β-benzyloxyaspartate (25 μM) led to a significant increase in cell participation in both layers, indicating that the concentration of extrasynaptic glutamate affects cell participation in both the INL and GCL. In contrast, blocking inhibitory transmission with the GABAA receptor antagonist gabazine and the glycine receptor antagonist strychnine increased cell participation in the GCL without significantly affecting the INL. These data indicate that during development, glutamate spillover provides a spatially diffuse source of depolarization, but that inhibitory circuits dictate which neurons within the GCL participate in retinal waves.
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Almeida, Norma A. S., Aline Cordeiro, Danielle S. Machado, Luana L. Souza, Tânia M. Ortiga-Carvalho, Antonio C. Campos-de-Carvalho, Fredric E. Wondisford, and Carmen C. Pazos-Moura. "Connexin40 Messenger Ribonucleic Acid Is Positively Regulated by Thyroid Hormone (TH) Acting in Cardiac Atria via the TH Receptor." Endocrinology 150, no. 1 (September 11, 2008): 546–54. http://dx.doi.org/10.1210/en.2008-0451.
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Thyroid hormone (TH) regulates many cardiac genes via nuclear thyroid receptors, and hyperthyroidism is frequently associated with atrial fibrillation. Electrical activity propagation in myocardium depends on the transfer of current at gap junctions, and connexins (Cxs) 40 and 43 are the predominant junction proteins. In mice, Cx40, the main Cx involved in atrial conduction, is restricted to the atria and fibers of the conduction system, which also express Cx43. We studied cardiac expression of Cx40 and Cx43 in conjunction with electrocardiogram studies in mice overexpressing the dominant negative mutant thyroid hormone receptor-β Δ337T exclusively in cardiomyocytes [myosin heavy chain (MHC-mutant)]. These mice develop the cardiac hypothyroid phenotype in the presence of normal serum TH. Expression was also examined in wild-type mice rendered hypothyroid or hyperthyroid by pharmacological treatment. Atrial Cx40 mRNA and protein levels were decreased (85 and 55%, respectively; P < 0.001) in MHC-mt mice. Atrial and ventricular Cx43 mRNA levels were not significantly changed. Hypothyroid and hyperthyroid animals showed a 25% decrease and 40% increase, respectively, in Cx40 mRNA abundance. However, MHC-mt mice presented very low Cx40 mRNA expression regardless of whether they were made hypothyroid or hyperthyroid. Atrial depolarization velocity, as represented by P wave duration in electrocardiograms of unanesthetized mice, was extremely reduced in MHC-mt mice, and to a lesser extent also in hypothyroid mice (90 and 30% increase in P wave duration). In contrast, this measure was increased in hyperthyroid mice (19% decrease in P wave duration). Therefore, this study reveals for the first time that Cx40 mRNA is up-regulated by TH acting in cardiac atria via the TH receptor and that this may be one of the mechanisms contributing to atrial conduction alterations in thyroid dysfunctions. Cardiac-specific expression of a mutant thyroid hormone receptor unable to bind thyroid hormone profoundly reduces atrial connexin 40 expression in association with prolonged atrial conduction.
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Duchen, Michael R., Anne Leyssens, and Martin Crompton. "Transient Mitochondrial Depolarizations Reflect Focal Sarcoplasmic Reticular Calcium Release in Single Rat Cardiomyocytes." Journal of Cell Biology 142, no. 4 (August 24, 1998): 975–88. http://dx.doi.org/10.1083/jcb.142.4.975.
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Digital imaging of mitochondrial potential in single rat cardiomyocytes revealed transient depolarizations of mitochondria discretely localized within the cell, a phenomenon that we shall call “flicker.” These events were usually highly localized and could be restricted to single mitochondria, but they could also be more widely distributed within the cell. Contractile waves, either spontaneous or in response to depolarization with 50 mM K+, were associated with propagating waves of mitochondrial depolarization, suggesting that propagating calcium waves are associated with mitochondrial calcium uptake and consequent depolarization. Here we demonstrate that the mitochondrial flicker was directly related to the focal release of calcium from sarcoplasmic reticular (SR) calcium stores and consequent uptake of calcium by local mitochondria. Thus, the events were dramatically reduced by (a) depletion of SR calcium stores after long-term incubation in EGTA or thapsigargin (500 nM); (b) buffering intracellular calcium using BAPTA-AM loading; (c) blockade of SR calcium release with ryanodine (30 μM); and (d) blockade of mitochondrial calcium uptake by microinjection of diaminopentane pentammine cobalt (DAPPAC), a novel inhibitor of the mitochondrial calcium uniporter. These observations demonstrate that focal SR calcium release results in calcium microdomains sufficient to promote local mitochondrial calcium uptake, suggesting a tight coupling of calcium signaling between SR release sites and nearby mitochondria.