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1
Alloway, K. D., M. B. Wallace, and M. J. Johnson. "Cross-correlation analysis of cuneothalamic interactions in the rat somatosensory system: influence of receptive field topography and comparisons with thalamocortical interactions." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1949–72. http://dx.doi.org/10.1152/jn.1994.72.4.1949.
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1. We simultaneously recorded neuronal responses to cutaneous stimulation from matched somatotopic representations in the nucleus cuneatus and ventrobasal complex of intact, halothane-anesthetized rats. A total of 95 cuneate and 86 thalamic neurons representing hairy skin on the forelimb were activated by hair movements produced by air jets at multiple skin sites. Mean responsiveness was higher among neurons in nucleus cuneatus (34.4 spikes per stimulus) than in thalamus (23.7 spikes per stimulus), a result that was consistent with the greater proportion of “sustained” responses recorded in nucleus cuneatus (80%) than in the thalamus (62%). 2. Cross-correlation analysis of 166 pairs of cuneate and thalamic neurons showed that 56 neuron pairs displayed time-locked correlations in activity that were characterized primarily by excitatory interactions (44 pairs) or a combination of excitatory and inhibitory interactions (10 pairs). Unilateral interactions in the cuneothalamic direction (31 pairs) and reverse direction (11 pairs) were observed, as well as multiphasic interactions in both directions (14 pairs). Most excitatory interactions involved intervals of 1–7 ms between successive cuneate and thalamic discharges, whereas most inhibitory influences involved intervals > 7 ms. Connection strength, defined by the ratio of time-linked interactions to the number of cuneate discharges, varied widely among neuron pairs but was largest for interactions involving interspike intervals of < or = 15 ms. 3. The relationship between connection strength and receptive field topography was analyzed in 103 cuneate-thalamic neuron pairs. The region of skin shared by both neurons varied substantially among neuron pairs and the probability of detecting interactions increased proportionately with larger amounts of receptive field overlap. Neuron pairs with moderate (25–50%) amounts of receptive field overlap had connection strengths 3–4 times greater than neuron pairs with minimal (0–25%) overlap. Connection strength was essentially identical, however, for neuron pairs with moderate or large (> 50%) amounts of overlap. 4. Cuneate-thalamic neuron pairs displaying functional connections were usually tested at multiple peripheral sites, but only 37% (18 of 49) of these neuron pairs displayed interactions at more than one stimulation site. Stimulation at different sites altered the timing of interactions in seven neuron pairs, including three that showed timing shifts across time zero in the cross-correlation histogram. In neuron pairs displaying interactions at multiple sites, connection strengths for 67% of the cases were strongest when stimulation was delivered within the region of receptive field overlap.(ABSTRACT TRUNCATED AT 400 WORDS)
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Pesavento, Michael J., Cynthia D. Rittenhouse, and David J. Pinto. "Response Sensitivity of Barrel Neuron Subpopulations to Simulated Thalamic Input." Journal of Neurophysiology 103, no. 6 (June 2010): 3001–16. http://dx.doi.org/10.1152/jn.01053.2009.
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Our goal is to examine the relationship between neuron- and network-level processing in the context of a well-studied cortical function, the processing of thalamic input by whisker-barrel circuits in rodent neocortex. Here we focus on neuron-level processing and investigate the responses of excitatory and inhibitory barrel neurons to simulated thalamic inputs applied using the dynamic clamp method in brain slices. Simulated inputs are modeled after real thalamic inputs recorded in vivo in response to brief whisker deflections. Our results suggest that inhibitory neurons require more input to reach firing threshold, but then fire earlier, with less variability, and respond to a broader range of inputs than do excitatory neurons. Differences in the responses of barrel neuron subtypes depend on their intrinsic membrane properties. Neurons with a low input resistance require more input to reach threshold but then fire earlier than neurons with a higher input resistance, regardless of the neuron's classification. Our results also suggest that the response properties of excitatory versus inhibitory barrel neurons are consistent with the response sensitivities of the ensemble barrel network. The short response latency of inhibitory neurons may serve to suppress ensemble barrel responses to asynchronous thalamic input. Correspondingly, whereas neurons acting as part of the barrel circuit in vivo are highly selective for temporally correlated thalamic input, excitatory barrel neurons acting alone in vitro are less so. These data suggest that network-level processing of thalamic input in barrel cortex depends on neuron-level processing of the same input by excitatory and inhibitory barrel neurons.
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Lytton, William W., Diego Contreras, Alain Destexhe, and Mircea Steriade. "Dynamic Interactions Determine Partial Thalamic Quiescence in a Computer Network Model of Spike-and-Wave Seizures." Journal of Neurophysiology 77, no. 4 (April 1, 1997): 1679–96. http://dx.doi.org/10.1152/jn.1997.77.4.1679.
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Lytton, William W., Diego Contreras, Alain Destexhe, and Mircea Steriade. Dynamic interactions determine partial thalamic quiescence in a computer network model of spike-and-wave seizures. J. Neurophysiol. 77: 1679–1696, 1997. In vivo intracellular recording from cat thalamus and cortex was performed during spontaneous spike-wave seizures characterized by synchronously firing cortical neurons correlated with the electroencephalogram. During these seizures, thalamic reticular (RE) neurons discharged with long spike bursts riding on a depolarization, whereas thalamocortical (TC) neurons were either entrained into the seizures (40%) or were quiescent (60%). During quiescence, TC neurons showed phasic inhibitory postsynaptic potentials (IPSPs) that coincided with paroxysmal depolarizing shifts in the simultaneously recorded cortical neuron. Computer simulations of a reciprocally connected TC-RE pair showed two major modes of TC-RE interaction. In one mode, a mutual oscillation involved direct TC neuron excitation of the RE neuron leading to a burst that fed back an IPSP into the TC neuron, producing a low-threshold spike. In the other, quiescent mode, the TC neuron was subject to stronger coalescing IPSPs. Simulated cortical stimulation could trigger a transition between the two modes. This transition could go in either direction and was dependent on the precise timing of the input. The transition did not always follow the stimulation immediately. A larger, multicolumnar simulation was set up to assess the role of the TC-RE pair in the context of extensive divergence and convergence. The amount of TC neuron spiking generally correlated with the strength of total inhibitory input, but large variations in the amount of spiking could be seen. Evidence for mutual oscillation could be demonstrated by comparing TC neuron firing with that in reciprocally connected RE neurons. An additional mechanism for TC neuron quiescence was assessed with the use of a cooperative model of γ-aminobutyric acid-B (GABAB)-mediated responses. With this model, RE neurons receiving repeated strong excitatory input produced TC neuron quiescence due to burst-duration-associated augmentation of GABAB current. We predict the existence of spatial inhomogeneity in apparently generalized spike-wave seizures, involving a center-surround pattern. In the center, intense cortical and RE neuron activity would be associated with TC neuron quiescence. In the surround, less intense hyperpolarization of TC neurons would allow low-threshold spikes to occur. This surround, an “epileptic penumbra,” would be the forefront of the expanding epileptic wave during the process of initial seizure generalization. Therapeutically, we would then predict that agents that reduce TC neuron activity would have a greater effect on seizure onset than on ongoing spike-wave seizures or other thalamic oscillations.
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Kasten, Michael R., and Matthew P. Anderson. "Self-regulation of adult thalamocortical neurons." Journal of Neurophysiology 114, no. 1 (July 2015): 323–31. http://dx.doi.org/10.1152/jn.00800.2014.
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The thalamus acts as a conduit for sensory and other information traveling to the cortex. In response to continuous sensory stimulation in vivo, the firing rate of thalamocortical neurons initially increases, but then within a minute firing rate decreases and T-type Ca2+ channel-dependent action potential burst firing emerges. While neuromodulatory systems could play a role in this inhibitory response, we instead report a novel and cell-autonomous inhibitory mechanism intrinsic to the thalamic relay neuron. Direct intracellular stimulation of thalamocortical neuron firing initially triggered a continuous and high rate of action potential discharge, but within a minute membrane potential ( Vm) was hyperpolarized and firing rate to the same stimulus was decreased. This self-inhibition was observed across a wide variety of thalamic nuclei, and in a subset firing mode switched from tonic to bursting. The self-inhibition resisted blockers of intracellular Ca2+ signaling, Na+-K+-ATPases, and G protein-regulated inward rectifier (GIRK) channels as implicated in other neuron subtypes, but instead was in part inhibited by an ATP-sensitive K+ channel blocker. The results identify a new homeostatic mechanism within the thalamus capable of gating excitatory signals at the single-cell level.
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Khatri, Vivek, Randy M. Bruno, and Daniel J. Simons. "Stimulus-Specific and Stimulus-Nonspecific Firing Synchrony and Its Modulation by Sensory Adaptation in the Whisker-to-Barrel Pathway." Journal of Neurophysiology 101, no. 5 (May 2009): 2328–38. http://dx.doi.org/10.1152/jn.91151.2008.
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The stimulus-evoked response of a cortical neuron depends on both details of the afferent signal and the momentary state of the larger network in which it is embedded. Consequently, identical sensory stimuli evoke highly variable responses. Using simultaneous recordings of thalamic barreloid and/or cortical barrel neurons in the rat whisker-to-barrel pathway, we determined the extent to which the responses of pairs of cells covary on a trial-by-trial basis. In the thalamus and cortical layer IV, a substantial component of trial-to-trial variability is independent of the specific parameters of the stimulus, probed here using deflection angle. These stimulus-nonspecific effects resulted in greater-than-chance similarities in trial-averaged angular tuning among simultaneously recorded pairs of barrel neurons. Such effects were not observed among simultaneously recorded thalamic and cortical barrel neurons, suggesting strong intracortical mechanisms of synchronization. Sensory adaptation produced by prior whisker deflections reduced response magnitudes and enhanced the joint angular tuning of simultaneously recorded neurons. Adaptation also decorrelated stimulus-evoked responses, rendering trial-by-trial responses of neuron pairs less similar to each other. Adaptation-induced decorrelation coupled with sharpened joint tuning could enhance the saliency of cells within thalamus or cortex that continue to fire synchronously during ongoing tactile stimulation associated with active touch.
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Azimirad, Vahid, and Mohammad Fattahi Sani. "Experimental Study of Reinforcement Learning in Mobile Robots Through Spiking Architecture of Thalamo-Cortico-Thalamic Circuitry of Mammalian Brain." Robotica 38, no. 9 (November 18, 2019): 1558–75. http://dx.doi.org/10.1017/s0263574719001632.
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SUMMARYIn this paper, the behavioral learning of robots through spiking neural networks is studied in which the architecture of the network is based on the thalamo-cortico-thalamic circuitry of the mammalian brain. According to a variety of neurons, the Izhikevich model of single neuron is used for the representation of neuronal behaviors. One thousand and ninety spiking neurons are considered in the network. The spiking model of the proposed architecture is derived and prepared for the learning problem of robots. The reinforcement learning algorithm is based on spike-timing-dependent plasticity and dopamine release as a reward. It results in strengthening the synaptic weights of the neurons that are involved in the robot’s proper performance. Sensory and motor neurons are placed in the thalamus and cortical module, respectively. The inputs of thalamo-cortico-thalamic circuitry are the signals related to distance of the target from robot, and the outputs are the velocities of actuators. The target attraction task is used as an example to validate the proposed method in which dopamine is released when the robot catches the target. Some simulation studies, as well as experimental implementation, are done on a mobile robot named Tabrizbot. Experimental studies illustrate that after successful learning, the meantime of catching target is decreased by about 36%. These prove that through the proposed method, thalamo-cortical structure could be trained successfully to learn to perform various robotic tasks.
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Viaene, Angela N., Iraklis Petrof, and S. Murray Sherman. "Synaptic Properties of Thalamic Input to Layers 2/3 and 4 of Primary Somatosensory and Auditory Cortices." Journal of Neurophysiology 105, no. 1 (January 2011): 279–92. http://dx.doi.org/10.1152/jn.00747.2010.
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We studied the synaptic profile of thalamic inputs to cells in layers 2/3 and 4 of primary somatosensory (S1) and auditory (A1) cortices using thalamocortical slices from mice age postnatal days 10–18. Stimulation of the ventral posterior medial nucleus (VPM) or ventral division of the medial geniculate body (MGBv) resulted in two distinct classes of responses. The response of all layer 4 cells and a minority of layers 2/3 cells to thalamic stimulation was Class 1, including paired-pulse depression, all-or-none responses, and the absence of a metabotropic component. On the other hand, the majority of neurons in layers 2/3 showed a markedly different, Class 2 response to thalamic stimulation: paired-pulse facilitation, graded responses, and a metabotropic component. The Class 1 and Class 2 response characteristics have been previously seen in inputs to thalamus and have been described as drivers and modulators, respectively. Driver input constitutes a main information bearing pathway and determines the receptive field properties of the postsynaptic neuron, whereas modulator input influences the response properties of the postsynaptic neuron but is not a primary information bearing input. Because these thalamocortical projections have comparable properties to the drivers and modulators in thalamus, we suggest that a driver/modulator distinction may also apply to thalamocortical projections. In addition, our data suggest that thalamus is likely to be more than just a simple relay of information and may be directly modulating cortex.
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Thomas, Elizabeth, and Thierry Grisar. "Increased Synchrony with Increase of a Low-Threshold Calcium Conductance in a Model Thalamic Network: A Phase-Shift Mechanism." Neural Computation 12, no. 7 (July 1, 2000): 1553–71. http://dx.doi.org/10.1162/089976600300015268.
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A computer model of a thalamic network was used in order to examine the effects of an isolated augmentation in a low-threshold calcium current. Such an isolated augmentation has been observed in the reticular thalamic (RE) nucleus of the genetic absence epilepsy rat from the Strasbourg (GAERS) model of absence epilepsy. An augmentation of the low-threshold calcium conductance in the RE neurons (gTs) of the model thalamic network was found to lead to an increase in the synchronized firing of the network. This supports the hypothesis that the isolated increase in gTs may be responsible for epileptic activity in the GAERS rat. The increase of gTs in the RE neurons led to a slight increase in the period of the isolated RE neuron firing. In contrast, the low-threshold spike of the RE neuron remained relatively unchanged by the increase of gTs. This suggests that the enhanced synchrony in the network was primarily due to a phase shift in the firing of the RE neurons with respect to the thalamocortical neurons. The ability of this phase-shift mechanism to lead to changes in synchrony was further examined using the model thalamic network. A similar increase in the period of RE neuron oscillations was obtained through an increase in the conductance of the calcium-mediated potassium channel. This change was once again found to increase synchronous firing in the network.
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Johnson, M. J., and K. D. Alloway. "Cross-correlation analysis reveals laminar differences in thalamocortical interactions in the somatosensory system." Journal of Neurophysiology 75, no. 4 (April 1, 1996): 1444–57. http://dx.doi.org/10.1152/jn.1996.75.4.1444.
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1. Spontaneous and stimulus-induced activity were recorded from corresponding somatotopic representations in the ventroposterolateral nucleus (VPL) of the thalamus and primary somatosensory (SI) cortex of intact, halothane-anesthetized cats. Thalamic and cortical neurons with overlapping receptive fields on the hairy skin of the forelimb were excited by a series of interleaved air jets aimed at multiple skin sites. 2. The laminar locations of 68% (240 of 355) of the neurons recorded in SI cortex were histologically reconstructed and responses of these 240 SI neurons were analyzed with respect to responses recorded from 118 thalamic neurons. Maximum responsiveness during the initial onset (1st 100 ms) of air jet stimulation was similar for neurons distributed throughout all layers of SI cortex (2-4 spikes per stimulus) and did not differ significantly from VPL responses. During the subsequent plateau phase of the stimulus, VPL neurons discharged at a mean rate of 19.0 spikes/ s and neurons in cortical layers II, IIIa, IIIb, and IV discharged at similar rates. Mean responsiveness during the plateau phase of the stimulus was significantly reduced among neurons in cortical layers V and VI and only averaged 7.1 and 3.9 spikes/s, respectively. 3. Responses recorded simultaneously from pairs of thalamic and cortical neurons were analyzed with cross-correlation analysis to determine differences in the incidence and strength of neuronal interactions as a function of cortical layer. Among 421 thalamocortical neuron pairs displaying stimulus-induced responses, 68 neuron pairs exhibited significant interactions during air jet stimulation. A laminar analysis revealed that 28% (45 of 163) of the neurons in the middle cortical layers displayed significant interactions with thalamic neurons, whereas only 14% (13 of 92) of superficial layer neurons and 6% (10 of 166) of deep layer neurons were synchronized with thalamic activity during air jet stimulation. When thalamocortical efficacy for different layers of cortex was plotted as a cumulative frequency distribution, the strongest interactions in the middle cortical layers were twice as strong as interactions involving the superficial or deep cortical layers. 4. More than 70% of stimulus-induced interactions involved thalamic discharges followed by subsequent cortical discharges and the majority of these interactions involved interspike intervals of < or = 3 ms. Nearly 75% (27 of 37) of interactions in the thalamocortical direction that involved cortical neurons in layers IIIb and IV transpired within a 3-ms interspike interval. For interactions with superficial or deep cortical layers, the proportion of thalamocortical interactions transpiring within 3 ms was only 58% (7 of 12) and 33% (2 of 6), respectively. 5. Cross-correlation analysis of spontaneous activity indicated that 124 pairs of thalamic and cortical neurons displayed synchronous activity in the absence of sensory stimulation. A laminar analysis indicated that similar proportions of cortical neurons in each layer were synchronized with thalamic activity in the absence of cutaneous stimulation. Thus 27% (44 of 163) of middle layer neurons, 30% (28 of 92) of superficial layer neurons, and 31% (51 of 166) of deep layer neurons displayed spontaneous interactions with thalamic neurons. The temporal pattern of spontaneous activity was examined with autocorrelation analysis to determine whether neuronal oscillations were essential for coordinating thalamic and cortical activity in the absence of peripheral stimulation. Only 18.5% (23 of 124) of spontaneous interactions between thalamic and cortical neurons were associated with periodic activity, which suggests that thalamocortical synchronization occurs before the constituent neurons begin to oscillate. 6. The influence of sensory stimulation on spontaneous interactions was examined in 31 pairs of thalamic and cortical neurons that exhibited interactions during prestimulus and stimulus in
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Goldberg, Jesse H., Michael A. Farries, and Michale S. Fee. "Integration of cortical and pallidal inputs in the basal ganglia-recipient thalamus of singing birds." Journal of Neurophysiology 108, no. 5 (September 1, 2012): 1403–29. http://dx.doi.org/10.1152/jn.00056.2012.
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The basal ganglia-recipient thalamus receives inhibitory inputs from the pallidum and excitatory inputs from cortex, but it is unclear how these inputs interact during behavior. We recorded simultaneously from thalamic neurons and their putative synaptically connected pallidal inputs in singing zebra finches. We find, first, that each pallidal spike produces an extremely brief (∼5 ms) pulse of inhibition that completely suppresses thalamic spiking. As a result, thalamic spikes are entrained to pallidal spikes with submillisecond precision. Second, we find that the number of thalamic spikes that discharge within a single pallidal interspike interval (ISI) depends linearly on the duration of that interval but does not depend on pallidal activity prior to the interval. In a detailed biophysical model, our results were not easily explained by the postinhibitory “rebound” mechanism previously observed in anesthetized birds and in brain slices, nor could most of our data be characterized as “gating” of excitatory transmission by inhibitory pallidal input. Instead, we propose a novel “entrainment” mechanism of pallidothalamic transmission that highlights the importance of an excitatory conductance that drives spiking, interacting with brief pulses of pallidal inhibition. Building on our recent finding that cortical inputs can drive syllable-locked rate modulations in thalamic neurons during singing, we report here that excitatory inputs affect thalamic spiking in two ways: by shortening the latency of a thalamic spike after a pallidal spike and by increasing thalamic firing rates within individual pallidal ISIs. We present a unifying biophysical model that can reproduce all known modes of pallidothalamic transmission—rebound, gating, and entrainment—depending on the amount of excitation the thalamic neuron receives.
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Zhang, Yusheng, Shihui Xing, Jian Zhang, Jingjing Li, Chuo Li, Zhong Pei, and Jinsheng Zeng. "Reduction of β-Amyloid Deposits by γ-Secretase Inhibitor is Associated with the Attenuation of Secondary Damage in the Ipsilateral Thalamus and Sensory Functional Improvement after Focal Cortical Infarction in Hypertensive Rats." Journal of Cerebral Blood Flow & Metabolism 31, no. 2 (August 4, 2010): 572–79. http://dx.doi.org/10.1038/jcbfm.2010.127.
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Abnormal β-amyloid (Aβ) deposits in the thalamus have been reported after cerebral cortical infarction. In this study, we investigated the association of Aβ deposits, with the secondary thalamic damage after focal cortical infarction in rats. Thirty-six stroke-prone renovascular hypertensive rats were subjected to distal middle cerebral artery occlusion (MCAO) and then randomly divided into MCAO, vehicle, and N-[ N-(3,5-difluorophenacetyl)-l-alanyl]- S-phenylglycine t-butyl ester (DAPT) groups and 12 sham-operated rats as control. The DAPT was administered orally at 72 hours after MCAO. Seven days after MCAO, sensory function, neuron loss, and glial activation and proliferation were evaluated using adhesive removal test, Nissl staining, and immunostaining, respectively. Thalamic Aβ accumulation was evaluated using immunostaining and enzyme-linked immunosorbent assay (ELISA). Compared with vehicle group, the ipsilateral thalamic Aβ, neuronal loss, glial activation and proliferation, and the mean time to remove the stimulus from right forepaw significantly decreased in DAPT group. The mean time to remove the stimulus from the right forepaw and thalamic Aβ burden were both negatively correlated with the number of thalamic neurons. These findings suggest that Aβ deposits are associated with the secondary thalamic damage. Reduction of thalamic Aβ by γ-secretase inhibitor may attenuate the secondary damage and improve sensory function after cerebral cortical infarction.
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Gursky, Zachary H., and Anna Y. Klintsova. "Changes in Representation of Thalamic Projection Neurons within Prefrontal-Thalamic-Hippocampal Circuitry in a Rat Model of Third Trimester Binge Drinking." Brain Sciences 11, no. 3 (March 4, 2021): 323. http://dx.doi.org/10.3390/brainsci11030323.
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Alcohol exposure (AE) during the third trimester of pregnancy—a period known as the brain growth spurt (BGS)—could result in a diagnosis of a fetal alcohol spectrum disorder (FASD), a hallmark of which is impaired executive functioning (EF). Coordinated activity between prefrontal cortex and hippocampus is necessary for EF and thalamic nucleus reuniens (Re), which is required for prefrontal-hippocampal coordination, is damaged following high-dose AE during the BGS. The current experiment utilized high-dose AE (5.25 g/kg/day) during the BGS (i.e., postnatal days 4–9) of Long-Evans rat pups. AE reduces the number of neurons in Re into adulthood and selectively alters the proportion of Re neurons that simultaneously innervate both medial prefrontal cortex (mPFC) and ventral hippocampus (vHPC). The AE-induced change unique to Re→(mPFC + vHPC) projection neurons (neuron populations that innervate either mPFC or vHPC individually were unchanged) is not mediated by reduction in neuron number. These data are the first to examine mPFC-Re-HPC circuit connectivity in a rodent model of FASD, and suggest that both short-term AE-induced neuron loss and long-term changes in thalamic connectivity may be two distinct (but synergistic) mechanisms by which developmental AE can alter mPFC-Re-vHPC circuitry and impair EF throughout the lifespan.
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Shoykhet, Michael, and Daniel J. Simons. "Development of Thalamocortical Response Transformations in the Rat Whisker-Barrel System." Journal of Neurophysiology 99, no. 1 (January 2008): 356–66. http://dx.doi.org/10.1152/jn.01063.2007.
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Extracellular single-unit recordings were used to characterize responses of thalamic barreloid and cortical barrel neurons to controlled whisker deflections in 2, 3-, and 4-wk-old and adult rats in vivo under fentanyl analgesia. Results indicate that response properties of thalamic and cortical neurons diverge during development. Responses to deflection onsets and offsets among thalamic neurons mature in parallel, whereas among cortical neurons responses to deflection offsets become disproportionately smaller with age. Thalamic neuron receptive fields become more multiwhisker, whereas those of cortical neurons become more single-whisker. Thalamic neurons develop a higher degree of angular selectivity, whereas that of cortical neurons remains constant. In the temporal domain, response latencies decrease both in thalamic and cortical neurons, but the maturation time-course differs between the two populations. Response latencies of thalamic cells decrease primarily between 2 and 3 wk of life, whereas response latencies of cortical neurons decrease in two distinct steps—the first between 2 and 3 wk of life and the second between the fourth postnatal week and adulthood. Although the first step likely reflects similar subcortical changes, the second phase likely corresponds to developmental myelination of thalamocortical fibers. Divergent development of thalamic and cortical response properties indicates that thalamocortical circuits in the whisker-to-barrel pathway undergo protracted maturation after 2 wk of life and provides a potential substrate for experience-dependent plasticity during this time.
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Pesavento, Michael J., and David J. Pinto. "Network and neuronal membrane properties in hybrid networks reciprocally regulate selectivity to rapid thalamocortical inputs." Journal of Neurophysiology 108, no. 9 (November 1, 2012): 2452–72. http://dx.doi.org/10.1152/jn.00914.2011.
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Rapidly changing environments require rapid processing from sensory inputs. Varying deflection velocities of a rodent's primary facial vibrissa cause varying temporal neuronal activity profiles within the ventral posteromedial thalamic nucleus. Local neuron populations in a single somatosensory layer 4 barrel transform sparsely coded input into a spike count based on the input's temporal profile. We investigate this transformation by creating a barrel-like hybrid network with whole cell recordings of in vitro neurons from a cortical slice preparation, embedding the biological neuron in the simulated network by presenting virtual synaptic conductances via a conductance clamp. Utilizing the hybrid network, we examine the reciprocal network properties (local excitatory and inhibitory synaptic convergence) and neuronal membrane properties (input resistance) by altering the barrel population response to diverse thalamic input. In the presence of local network input, neurons are more selective to thalamic input timing; this arises from strong feedforward inhibition. Strongly inhibitory (damping) network regimes are more selective to timing and less selective to the magnitude of input but require stronger initial input. Input selectivity relies heavily on the different membrane properties of excitatory and inhibitory neurons. When inhibitory and excitatory neurons had identical membrane properties, the sensitivity of in vitro neurons to temporal vs. magnitude features of input was substantially reduced. Increasing the mean leak conductance of the inhibitory cells decreased the network's temporal sensitivity, whereas increasing excitatory leak conductance enhanced magnitude sensitivity. Local network synapses are essential in shaping thalamic input, and differing membrane properties of functional classes reciprocally modulate this effect.
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Lenz, F. A., C. J. Jaeger, M. S. Seike, Y. C. Lin, and S. G. Reich. "Single-Neuron Analysis of Human Thalamus in Patients With Intention Tremor and Other Clinical Signs of Cerebellar Disease." Journal of Neurophysiology 87, no. 4 (April 1, 2002): 2084–94. http://dx.doi.org/10.1152/jn.00049.2001.
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Tremor that occurs as a result of a cerebellar lesion, cerebellar tremor, is characteristically an intention tremor. Thalamic activity may be related to cerebellar tremor because transmission of some cerebellar efferent signals occurs via the thalamus and cortex to the periphery. We have now studied thalamic neuronal activity in a cerebellar relay nucleus (ventral intermediate—Vim) and a pallidal relay nucleus (ventralis oral posterior—Vop) during thalamotomy in patients with intention tremor and other clinical signs of cerebellar disease (tremor patients). The activity of single neurons and the simultaneous electromyographic (EMG) activity of the contralateral upper extremity in tremor patients performing a pointing task were analyzed by spectral cross-correlation analysis. EMG spectra during intention tremor often showed peaks of activity in the tremor-frequency range (1.9–5.8 Hz). There were significant differences in thalamic neuronal activity between tremor patients and controls. Neurons in Vim and Vop had significantly lower firing rates in tremor patients than in patients undergoing thalamic surgery for pain (pain controls). Other studies have shown that inputs to Vim from the cerebellum are transmitted through excitatory connections. Therefore the present results suggest that tremor in these tremor patients is associated with deafferentation of the thalamus from cerebellar efferent pathways. The thalamic X EMG cross-correlation functions were studied for cells located in Vim and Vop. Neuronal and EMG activity were as likely to be significantly correlated for cells in Vim as for those in Vop. Cells in Vim were more likely to have a phase lag relative to EMG than were cells in Vop. In monkeys, cells in the cerebellar relay nucleus of the thalamus, corresponding to Vim, are reported to lead movement during active oscillations at the wrist. In view of these monkey studies, the present results suggest that cells in Vim are deafferented and have a phase lag relative to tremor that is not found in normal active oscillations. The difference in phase of thalamic spike X EMG activity between Vim and Vop may contribute to tremor because lesions of pallidum or Vop are reported to relieve cerebellar tremor.
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Deymeer, F., T. W. Smith, U. DeGirolami, and D. A. Drachman. "Thalamic dementia and motor neuron disease." Neurology 39, no. 1 (January 1, 1989): 58. http://dx.doi.org/10.1212/wnl.39.1.58.
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Crunelli, Vincenzo, Kate L. Blethyn, David W. Cope, Stuart W. Hughes, H. Rheinallt Parri, Jonathan P. Turner, Tibor I. Tòth, and Stephen R. Williams. "Novel neuronal and astrocytic mechanisms in thalamocortical loop dynamics." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 357, no. 1428 (December 29, 2002): 1675–93. http://dx.doi.org/10.1098/rstb.2002.1155.
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In this review, we summarize three sets of findings that have recently been observed in thalamic astrocytes and neurons, and discuss their significance for thalamocortical loop dynamics. (i) A physiologically relevant ‘window’ component of the low–voltage–activated, T–type Ca 2+ current ( I Twindow ) plays an essential part in the slow (less than 1 Hz) sleep oscillation in adult thalamocortical (TC) neurons, indicating that the expression of this fundamental sleep rhythm in these neurons is not a simple reflection of cortical network activity. It is also likely that I Twindow underlies one of the cellular mechanisms enabling TC neurons to produce burst firing in response to novel sensory stimuli. (ii) Both electrophysiological and dye–injection experiments support the existence of gap junction–mediated coupling among young and adult TC neurons. This finding indicates that electrical coupling–mediated synchronization might be implicated in the high and low frequency oscillatory activities expressed by this type of thalamic neuron. (iii) Spontaneous intracellular Ca 2+ ([Ca 2+ ] i ) waves propagating among thalamic astrocytes are able to elicit large and long–lasting N –methyl–D–aspartate–mediated currents in TC neurons. The peculiar developmental profile within the first two postnatal weeks of these astrocytic [Ca 2+ ] i transients and the selective activation of these glutamate receptors point to a role for this astrocyte–to–neuron signalling mechanism in the topographic wiring of the thalamocortical loop. As some of these novel cellular and intracellular properties are not restricted to thalamic astrocytes and neurons, their significance may well apply to (patho)physiological functions of glial and neuronal elements in other brain areas.
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Kwegyir-Afful, E. E., H. T. Kyriazi, and D. J. Simons. "Weaker feedforward inhibition accounts for less pronounced thalamocortical response transformation in mouse vs. rat barrels." Journal of Neurophysiology 110, no. 10 (November 15, 2013): 2378–92. http://dx.doi.org/10.1152/jn.00574.2012.
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Feedforward inhibition is a common motif of thalamocortical circuits. Strong engagement of inhibitory neurons by thalamic inputs enhances response differentials between preferred and nonpreferred stimuli. In rat whisker-barrel cortex, robustly driven inhibitory barrel neurons establish a brief epoch during which synchronous or near-synchronous thalamic firing produces larger responses to preferred stimuli, such as high-velocity deflections of the principal whisker in a preferred direction. Present experiments in mice show that barrel neuron responses to preferred vs. nonpreferred stimuli differ less than in rats. In addition, fast-spike units, thought to be inhibitory barrel neurons, fire less robustly to whisker stimuli in mice than in rats. Analyses of real and simulated data indicate that mouse barrel circuitry integrates thalamic inputs over a broad temporal window, and that, as a consequence, responses of barrel neurons are largely similar to those of thalamic neurons. Results are consistent with weaker feedforward inhibition in mouse barrels. Differences in thalamocortical circuitry between mice and rats may reflect mechanical properties of the whiskers themselves.
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Verhagen, Justus V., Barbara K. Giza, and Thomas R. Scott. "Effect of Amiloride on Gustatory Responses in the Ventroposteromedial Nucleus of the Thalamus in Rats." Journal of Neurophysiology 93, no. 1 (January 2005): 157–66. http://dx.doi.org/10.1152/jn.00823.2003.
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The existence of gustatory neuron types has been demonstrated in the chorda tympani nerve and the nucleus of the solitary tract (NTS) of rats and hamsters through the oral application of amiloride, a sodium channel blocker. At these lower-order levels, amiloride was shown to reduce the response to sodium and lithium salts in sodium- and sugar-oriented cells, while leaving those of acid- and quinine-oriented neurons unmodified. We extended this investigation to higher-order levels by determining whether amiloride suppressed the responses of cells at the 4th-order gustatory relay in the thalamus, which neurons were affected, the degree of suppression, and whether the subsequent neural code for sodium was altered. We stimulated the whole oral cavity of anesthetized rats with a variety of tastants while recording the responses of 42 single thalamic neurons before and after the application of amiloride. The results revealed a similar pattern to that reported in the NTS. Amiloride inhibited only sodium- and sugar-oriented neurons, and specifically their responses to sodium- or lithium-containing stimuli. Moreover, there was a significant relationship between the degree of sodium specificity of a neuron and its sensitivity to inhibition by amiloride. These results demonstrate a relationship between a cell's response profile and its susceptibility to amiloride, and so offer evidence that gustatory neuron types exist through the level of the thalamus in rats. Thus membership in a neuronal group retains functional significance based on a receptor event 4 synapses away.
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Yoshioka, Takashi, Jonathan B. Levitt, and Jennifer S. Lund. "Independence and merger of thalamocortical channels within macaque monkey primary visual cortex: Anatomy of interlaminar projections." Visual Neuroscience 11, no. 3 (May 1994): 467–89. http://dx.doi.org/10.1017/s0952523800002406.
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AbstractAn important issue in understanding the function of primary visual cortex in the macaque monkey is how the several efferent neuron groups projecting to extrastriate cortex acquire their different response properties. To assist our understanding of this issue, we have compared the anatomical distribution of VI intrinsic relays that carry information derived from magno- (M) and parvocellular (P) divisions of the dorsal lateral geniculate nucleus between thalamic recipient neurons and interareal efferent neuron groups within area VI. We used small, iontophoretic injections of biocytin placed in individual cortical laminae of area VI to trace orthograde and retrograde inter- and intralaminar projections. In either the same or adjacent sections, the tissue was reacted for cytochrome oxidase (CO), which provides important landmarks for different efferent neuron populations located in CO rich blobs and CO poor interblobs in laminae ⅔, as well as defining clear boundaries for the populations of efferent neurons in laminae 4A and 4B. This study shows that the interblobs, but not the blobs, receive direct input from thalamic recipient 4C neurons; the interblobs receive relays from mid 4C neurons (believed to receive convergent M and P inputs), while blobs receive indirect inputs from either M or P (or both) pathways through layers 4B (which receives M relays from layer 4Cα) and 4A (which receives P relays directly from the thalamus as well as from layer 4Cβ). The property of orientation selectivity, most prominent in the interblob regions and in layer 4B, may have a common origin from oriented lateral projections made by mid 4C spiny stellate neurons. While layer 4B efferents may emphasize M characteristics and layer 4A efferents emphasize P characteristics, the dendrites of their constituent pyramidal neurons may provide anatomical access to the other channel since both blob and interblob regions in layers ⅔ have anatomical access to M and P driven relays, despite functional differences in the way these properties may be expressed in the two compartments.
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Pinto, David J., Joshua C. Brumberg, and Daniel J. Simons. "Circuit Dynamics and Coding Strategies in Rodent Somatosensory Cortex." Journal of Neurophysiology 83, no. 3 (March 1, 2000): 1158–66. http://dx.doi.org/10.1152/jn.2000.83.3.1158.
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Previous experimental studies of both cortical barrel and thalamic barreloid neuron responses in rodent somatosensory cortex have indicated an active role for barrel circuitry in processing thalamic signals. Previous modeling studies of the same system have suggested that a major function of the barrel circuit is to render the response magnitude of barrel neurons particularly sensitive to the temporal distribution of thalamic input. Specifically, thalamic inputs that are initially synchronous strongly engage recurrent excitatory connections in the barrel and generate a response that briefly withstands the strong damping effects of inhibitory circuitry. To test this experimentally, we recorded responses from 40 cortical barrel neurons and 63 thalamic barreloid neurons evoked by whisker deflections varying in velocity and amplitude. This stimulus evoked thalamic response profiles that varied in terms of both their magnitude and timing. The magnitude of the thalamic population response, measured as the average number of evoked spikes per stimulus, increased with both deflection velocity and amplitude. On the other hand, the degree of initial synchrony, measured from population peristimulus time histograms, was highly correlated with the velocity of whisker deflection, deflection amplitude having little or no effect on thalamic synchrony. Consistent with the predictions of the model, the cortical population response was determined largely by whisker velocity and was highly correlated with the degree of initial synchrony among thalamic neurons ( R 2 = 0.91), as compared with the average number of evoked thalamic spikes ( R 2 = 0.38). Individually, the response of nearly all cortical cells displayed a positive correlation with deflection velocity; this homogeneity is consistent with the dependence of the cortical response on local circuit interactions as proposed by the model. By contrast, the response of individual thalamic neurons varied widely. These findings validate the predictions of the modeling studies and, more importantly, demonstrate that the mechanism by which the cortex processes an afferent signal is inextricably linked with, and in fact determines, the saliency of neural codes embedded in the thalamic response.
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Shu, Yousheng, and David A. McCormick. "Inhibitory Interactions Between Ferret Thalamic Reticular Neurons." Journal of Neurophysiology 87, no. 5 (May 1, 2002): 2571–76. http://dx.doi.org/10.1152/jn.00850.2001.
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The thalamic reticular nucleus (nRt) provides an important inhibitory input to thalamic relay nuclei and is central in the generation of both normal and abnormal thalamocortical activities. Although local inhibitory interactions between these neurons may play an important role in controlling thalamocortical activities, the physiological features of this interaction have not been fully investigated. Here we sought to establish the nature of inhibitory interaction between nRt neurons with intracellular and extracellular recordings in slices of ferret nRt maintained in vitro. In many nRt neurons, intracellular recordings revealed spontaneous inhibitory postsynaptic potentials (IPSPs). In addition, the local excitation of nRt cells with glutamate led to the generation of IPSPs in the intracellularly recorded nRt neuron. These evoked IPSPs exhibited an average reversal potential of −72 mV and could be blocked by picrotoxin, a GABAA-receptor antagonist. These results indicate that nRt neurons interact locally through the activation of GABAA receptor-mediated inhibitory postsynaptic potentials. This lateral inhibition may play an important role in controlling the responsiveness of these cells to cortical and thalamic excitatory inputs in both normal and abnormal thalamocortical function.
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Govindaiah, G., and Charles L. Cox. "Modulation of thalamic neuron excitability by orexins." Neuropharmacology 51, no. 3 (September 2006): 414–25. http://dx.doi.org/10.1016/j.neuropharm.2006.03.030.
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Alloway, K. D., M. J. Johnson, and M. B. Wallace. "Thalamocortical interactions in the somatosensory system: interpretations of latency and cross-correlation analyses." Journal of Neurophysiology 70, no. 3 (September 1, 1993): 892–908. http://dx.doi.org/10.1152/jn.1993.70.3.892.
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1. Isolated extracellular neuronal responses to cutaneous stimulation were simultaneously recorded from corresponding peripheral representations in the ventrobasal nucleus and primary somatosensory cortex of intact, halothane-anesthetized rats. Thalamic and cortical neurons representing hairy skin on the forelimb were activated by hair movements produced by a series of 50 or 100 discrete air jets. A corresponding set of neurons representing the glabrous pads of the hind paw were activated by a similar number of punctate mechanical displacements. 2. Cortical electrode penetrations were histologically reconstructed, and 118 neurons in the glabrous skin representation exhibited cutaneous responses that were categorized into supragranular, granular, or infragranular groups according to their laminar position. Minimum latencies of cortical neurons responding to glabrous skin displacement were analyzed, and significant differences were found in the distribution of minimum latencies for the different cortical layers. Mean values for minimum latencies in the infragranular and granular layers were 15.8 and 16.3 ms, respectively, whereas supragranular neurons were characterized by minimum latencies having a mean of 20 ms. The differences between these groups suggests that stimulus-induced afferent activity reaches infragranular and granular layers before contacting supragranular neurons. Average latencies were also calculated on responses occurring during the 1st 20 trials, but the cortical distributions of these values overlapped considerably, and differences between the laminar groups were not statistically significant. 3. In several recording sites, two cortical neurons were recorded simultaneously, and the response latencies of these matched pairs were often substantially different despite the similarity in laminar position. This result indicates that laminar location is not the only determinant of response latency and that serially organized circuits are distributed within, as well as between, cortical layers. 4. From a sample of 302 neurons exhibiting cutaneous responses within histologically identified regions of thalamus or cortex, a set of 143 pairs of neurons recorded simultaneously from both regions was available for cross-correlation analysis. Significant thalamocortical interactions were found in 38 neurons pairs. Analysis of these significant interactions revealed that thalamocortical connection strength, as measured by neuronal efficacy, was two to four times larger for neuron pairs having the cortical cell in granular layer IV than for neuron pairs having an extragranular layer cortical neuron. There was no difference in thalamocortical connection strength between neuron pairs containing supra- or infragranular cortical neurons. 5. Summed peristimulus time histograms revealed stimulus-locked inhibition of spontaneous activity in 4% (8/195) or cortical and 18% (20/107) of thalamic neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
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Lu, Meili, Yingmei Qin, Huiyan Li, Yanqiu Che, Chunxiao Han, and Xile Wei. "Calcium conductance-dependent network synchronization is differentially modulated by firing frequency." International Journal of Modern Physics B 33, no. 15 (June 20, 2019): 1950160. http://dx.doi.org/10.1142/s0217979219501601.
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Synchronous oscillations in certain frequencies of the sub-thalamic nucleus (STN) neurons are closely related to the physical symptoms of Parkinson’s disease (PD). Recent results have highlighted the importance of calcium channels in the synchronization properties and regulation of STN neurons. In this paper, a novel hybrid neuron model which can capture the electrophysiological signature of neurons with low or high density of calcium channels is used to explore the synchronization propensity and regulation by firing frequencies of neurons. Numerical simulations show that the synchronization propensity of networks consisting of the novel hybrid neurons is quite distinguishing in low and high calcium conductance modes, especially, the synchronization can be differentially modulated by network frequencies in the two modes. By analyzing the firing frequency and phase response curve of the individual neuron, we find that a single parameter of the hybrid neuron, which is a direct image of the calcium conductance, is crucial in determining the excitability and response properties of the neuron. Different phase response properties of single neurons in different calcium conductance modes lead to network synchronization discrepancies.
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Herrero-Navarro, Álvaro, Lorenzo Puche-Aroca, Verónica Moreno-Juan, Alejandro Sempere-Ferràndez, Ana Espinosa, Rafael Susín, Laia Torres-Masjoan, et al. "Astrocytes and neurons share region-specific transcriptional signatures that confer regional identity to neuronal reprogramming." Science Advances 7, no. 15 (April 2021): eabe8978. http://dx.doi.org/10.1126/sciadv.abe8978.
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Neural cell diversity is essential to endow distinct brain regions with specific functions. During development, progenitors within these regions are characterized by specific gene expression programs, contributing to the generation of diversity in postmitotic neurons and astrocytes. While the region-specific molecular diversity of neurons and astrocytes is increasingly understood, whether these cells share region-specific programs remains unknown. Here, we show that in the neocortex and thalamus, neurons and astrocytes express shared region-specific transcriptional and epigenetic signatures. These signatures not only distinguish cells across these two brain regions but are also detected across substructures within regions, such as distinct thalamic nuclei, where clonal analysis reveals the existence of common nucleus-specific progenitors for neurons and astrocytes. Consistent with their shared molecular signature, regional specificity is maintained following astrocyte-to-neuron reprogramming. A detailed understanding of these regional-specific signatures may thus inform strategies for future cell-based brain repair.
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Golomb, D., X. J. Wang, and J. Rinzel. "Synchronization properties of spindle oscillations in a thalamic reticular nucleus model." Journal of Neurophysiology 72, no. 3 (September 1, 1994): 1109–26. http://dx.doi.org/10.1152/jn.1994.72.3.1109.
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1. We address the hypothesis of Steriade and colleagues that the thalamic reticular nucleus (RE) is a pacemaker for thalamocortical spindle oscillations by developing and analyzing a model of a large population of all-to-all coupled inhibitory RE neurons. 2. Each RE neuron has three ionic currents: a low-threshold T-type Ca2+ current (ICa-T), a calcium-activated potassium current (IAHP) and a leakage current (IL). ICa-T underlies a cell's postinhibitory rebound properties, whereas IAHP hyperpolarizes the neuron after a burst. Each neuron, which is a conditional oscillator, is coupled to all other RE neurons via fast gamma-aminobutyric acid-A (GABAA) and slow GABAB synapses. 3. For generating network oscillations IAHP may not be necessary. Synaptic inhibition can provide the hyperpolarization for deinactivating ICa-T that causes bursting if the reversal potentials for GABAA and GABAB synapses are sufficiently negative. 4. If model neurons display sufficiently powerful rebound excitability, an isolated RE network of such neurons oscillates with partial but typically not full synchrony. The neurons spontaneously segregate themselves into several macroscopic clusters. The neurons within a cluster follow the same time course, but the clusters oscillate differently from one another. In addition to activity patterns in which clusters burst sequentially (e.g., 2 or 3 clusters bursting alternately), a two-cluster state may occur with one cluster active and one quiescent. Because the neurons are all-to-all coupled, the cluster states do not have any spatial structure. 5. We have explored the sensitivity of such partially synchronized patterns to heterogeneity in cells' intrinsic properties and to simulated neuroelectric noise. Although either precludes precise clustering, modest levels of heterogeneity or noise lead to approximate clustering of active cells. The population-averaged voltage may oscillate almost regularly but individual cells burst at nearly every second cycle or less frequently. The active-quiescent state is not robust at all to heterogeneity or noise. Total asynchrony is observed when heterogeneity or noise is too large, e.g., even at 25% heterogeneity for our reference set of parameter values. 6. The fast GABAA inhibition (with a reversal potential more negative than, say, -65 mV) favors the cluster states and prevents full synchrony. Our simulation results suggest two mechanisms that can fully synchronize the isolated RE network model. With GABAA removed or almost totally blocked, GABAB inhibition (because it is slow) can lead to full synchrony, which is partially robust to heterogeneity and noise.(ABSTRACT TRUNCATED AT 400 WORDS)
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Moreno, Sandra, Roberta Nardacci, and Maria Paola Cerù. "Regional and Ultrastructural Immunolocalization of Copper-Zinc Superoxide Dismutase in Rat Central Nervous System." Journal of Histochemistry & Cytochemistry 45, no. 12 (December 1997): 1611–22. http://dx.doi.org/10.1177/002215549704501204.
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We examined the distribution of copper-zinc superoxide dismutase (CuZn-SOD) in adult rat central nervous system by light and electron microscopic immunocytochemistry, using an affinity-purified polyclonal antibody. The enzyme appeared to be exclusively localized in neurons. No immunoreactivity was seen in non-neuronal cells. The staining intensity was variable, depending on the brain region and, within the same region, on the neuron type. Highly immunoreactive elements included cortical neurons evenly distributed in the different layers, hippocampal interneurons, neurons of the reticular thalamic nucleus, and Golgi, stellate, and basket cells of the cerebellar cortex. Other neurons, i.e., pyramidal cells of the neocortex and hippocampus, Purkinje and granule cells of the cerebellar cortex, and the majority of thalamic neurons, showed much weaker staining. In the spinal cord, intense CuZnSOD immunoreactivity was present in many neurons, including motor neurons. Pre-embedding immunoelectron microscopy of the neocortex, hippocampus, reticular thalamic nucleus, and cerebellar cortex showed cytosolic and nucleoplasmic labeling. Moreover, single membrane-limited immunoreactive organelles identified as peroxisomes were often found, even in neurons that appeared weakly stained at the light microscopic level. In double immunogold labeling experiments, particulate CuZn-SOD immunoreactivity co-localized with catalase, a marker enzyme for peroxisomes, thus demonstrating that in neural tissue CuZnSOD is also present in peroxisomes.
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Lenz, F. A., C. J. Jaeger, M. S. Seike, Y. C. Lin, S. G. Reich, M. R. DeLong, and J. L. Vitek. "Thalamic Single Neuron Activity in Patients With Dystonia: Dystonia-Related Activity and Somatic Sensory Reorganization." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2372–92. http://dx.doi.org/10.1152/jn.1999.82.5.2372.
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Indirect evidence suggests that the thalamus contributes to abnormal movements occurring in patients with dystonia (dystonia patients). The present study tested the hypothesis that thalamic activity contributes to the dystonic movements that occur in such patients. During these movements, spectral analysis of electromyographic (EMG) signals in flexor and extensor muscles of the wrist and elbow exhibited peak EMG power in the lowest frequency band [0–0.78 Hz (mean: 0.39 Hz) dystonia frequency] for 60–85% of epochs studied during a pointing task. Normal controls showed low-frequency peaks for <16% of epochs during pointing. Among dystonia patients, simultaneous contraction of antagonistic muscles (cocontraction) at dystonia frequency during pointing was observed for muscles acting about the wrist (63% of epochs) and elbow (39%), but cocontraction was not observed among normal controls during pointing. Thalamic neuronal signals were recorded during thalamotomy for treatment of dystonia and were compared with those of control patients without motor abnormality who were undergoing thalamic procedures for treatment of chronic pain. Presumed nuclear boundaries of a human thalamic cerebellar relay nucleus (ventral intermediate, Vim) and a pallidal relay nucleus (ventral oral posterior, Vop) were estimated by aligning the anterior border of the principal sensory nucleus (ventral caudal, Vc) with the region where the majority of cells have cutaneous receptive fields (RFs). The ratio of power at dystonia frequency to average spectral power was >2 ( P < 0.001) for cells in presumed Vop often for dystonia patients (81%) but never for control patients. The percentage of such cells in presumed Vim of dystonia patients (32%) was not significantly different from that of controls (31%). Many cells in presumed Vop exhibited dystonia frequency activity that was correlated with and phase-advanced on EMG activity during dystonia, suggesting that this activity was related to dystonia. Thalamic somatic sensory activity also differed between dystonia patients and controls. The percentage of cells responding to passive joint movement or to manipulation of subcutaneous structures (deep sensory cells) in presumed Vim was significantly greater in patients with dystonia than in control patients undergoing surgery for treatment of pain or tremor. Dystonia patients had a significantly higher proportion of deep sensory cells responding to movement of more than one joint (26%, 13/52) than did “control” patients (8%, 4/49). Deep sensory cells in patients with dystonia were located in thalamic maps that demonstrated increased representations of parts of the body affected by dystonia. Thus dystonia patients showed increased receptive fields and an increased thalamic representation of dystonic body parts. The motor activity of an individual sensory cell was related to the sensory activity of that cell by identification of the muscle apparently involved in the cell's receptive field. Specifically, we defined the effector muscle as the muscle that, by contraction, produced the joint movement associated with a thalamic neuronal sensory discharge, when the examiner passively moved the joint. Spike X EMG correlation functions during dystonia indicated that thalamic cellular activity less often was related to EMG in effector muscles (52%) than in other muscles (86%). Thus there is a mismatch between the effector muscle for a thalamic cell and the muscles with EMG correlated with activity of that cell during dystonia. This mismatch may result from the reorganization of sensory maps and may contribute to the simultaneous activation of multiple muscles observed in dystonia. Microstimulation in presumed Vim in dystonia patients produced simultaneous contraction of multiple forearm muscles, similar to the simultaneous muscle contractions observed in dystonia. These observations are consistent with a model in which sensory input to Vim in dystonia is transmitted through altered sensory maps to activate multiple muscles in the periphery, producing the overflow of muscle activation that is characteristic of dystonia.
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Tanibuchi, Ikuo, Hiroyuki Kitano, and Kohnosuke Jinnai. "Substantia Nigra Output to Prefrontal Cortex Via Thalamus in Monkeys. I. Electrophysiological Identification of Thalamic Relay Neurons." Journal of Neurophysiology 102, no. 5 (November 2009): 2933–45. http://dx.doi.org/10.1152/jn.91287.2008.
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A few studies have been performed in primate basal ganglia–thalamo–prefrontal pathways. Nevertheless, their electrophysiological properties and anatomical arrangements remain obscure. This study examined them in nigro-thalamo-cortical pathways from the substantia nigra pars reticulata (SNr) to the frontal cortex (FRC) via the mediodorsal (MD) and ventral anterior (VA) thalamus in monkeys. First, single thalamocortical neurons with SNr input were identified by antidromic responses to FRC stimulation and by inhibitory orthodromic responses with short latencies (<5 ms) to SNr stimulation. Second, single nigrothalamic neurons were found by antidromic responses to stimulation of the portions of the MD and VA where the thalamocortical neurons were recorded. The inhibitory orthodromic responses in the thalamocortical neurons were considered to be monosynaptically induced by nigral stimulation because the latency distribution of the orthodromic responses in the thalamocortical neurons was similar to that of the antidromic responses in the nigrothalamic neurons. Almost all relay neurons in the rostrolateral MD received inhibitory afferents from the caudolateral SNr and projected to the prefrontal area ventral to the principal sulcus, which constituted the densest nigro-thalamo-cortical projections. Meanwhile, neurons in the VA received inhibitory signals from the whole rostrocaudal extent of the SNr and projected to wide regions of the FRC; neurons in its pars magnocellularis mostly projected to different prefrontal areas, while those in its pars parvocellularis projected to motor areas. This report substantiated the topography of thalamocortical neurons monosynaptically receiving inhibitory SNr input and projecting to the FRC in the primate MD and VA at the single-neuron level.
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Rush, Maureen E., and John Rinzel. "Analysis of bursting in a thalamic neuron model." Biological Cybernetics 71, no. 4 (August 1994): 281–91. http://dx.doi.org/10.1007/bf00239616.
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Gupta, Shruti, and Jyotsna Singh. "Effect of applied current on sub-thalamic neuron." CSI Transactions on ICT 4, no. 2-4 (December 2016): 183–85. http://dx.doi.org/10.1007/s40012-016-0120-1.
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Rush, Maureen E., and John Rinzel. "Analysis of bursting in a thalamic neuron model." Biological Cybernetics 71, no. 4 (August 1, 1994): 281–91. http://dx.doi.org/10.1007/s004220050090.
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Zhu, Zhi-ru, Fenglian Xu, Wei-gang Ji, Shuan-cheng Ren, Fang Chen, Peng-zhi Chen, Hui-hui Jiang, et al. "Synaptic mechanisms underlying thalamic activation-induced plasticity in the rat auditory cortex." Journal of Neurophysiology 111, no. 9 (May 1, 2014): 1746–58. http://dx.doi.org/10.1152/jn.00180.2013.
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Electrical stimulation of ventral division of medial geniculate body (MGBv) neurons evokes a shift of the frequency-tuning curves of auditory cortical (AC) neurons toward the best frequency (BF) of the stimulated MGBv neurons (frequency-specific plasticity). The shift of BF is induced by inhibition of responses at the BF of the recorded AC neuron, with coincident facilitation of responses at the BF of the stimulated MGBv neuron. However, the synaptic mechanisms are not yet understood. We hypothesize that activation of thalamocortical synaptic transmission and receptor function may contribute to MGBv stimulation-induced frequency-specific auditory plasticity and the shift of BF. To test this hypothesis, we measured changes in the excitatory postsynaptic currents in pyramidal neurons of layer III/IV in the auditory cortex following high-frequency stimulation (HFS) of the MGBv, using whole cell recordings in an auditory thalamocortical slice. Our data showed that in response to the HFS of the MGBv the excitatory postsynaptic currents of AC neurons showed long-term bidirectional synaptic plasticity and long-term potentiation and depression. Pharmacological studies indicated that the long-term synaptic plasticity was induced through the activation of different sets of N-methyl-d-aspartate-type glutamatergic receptors, γ-aminobutyric acid-type receptors, and type 5 metabotropic glutamate receptors. Our data further demonstrated that blocking of different receptors with specific antagonists significantly inhibited MGBv stimulation-induced long-term plasticity as well as the shift of BF. These data indicate that these receptors have an important role in mediating frequency-specific auditory cortical plasticity.
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Gribkova, Ekaterina D., Baher A. Ibrahim, and Daniel A. Llano. "A novel mutual information estimator to measure spike train correlations in a model thalamocortical network." Journal of Neurophysiology 120, no. 6 (December 1, 2018): 2730–44. http://dx.doi.org/10.1152/jn.00012.2018.
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The impact of thalamic state on information transmission to the cortex remains poorly understood. This limitation exists due to the rich dynamics displayed by thalamocortical networks and because of inadequate tools to characterize those dynamics. Here, we introduce a novel estimator of mutual information and use it to determine the impact of a computational model of thalamic state on information transmission. Using several criteria, this novel estimator, which uses an adaptive partition, is shown to be superior to other mutual information estimators with uniform partitions when used to analyze simulated spike train data with different mean spike rates, as well as electrophysiological data from simultaneously recorded neurons. When applied to a thalamocortical model, the estimator revealed that thalamocortical cell T-type calcium current conductance influences mutual information between the input and output from this network. In particular, a T-type calcium current conductance of ~40 nS appears to produce maximal mutual information between the input to this network (conceptualized as afferent input to the thalamocortical cell) and the output of the network at the level of a layer 4 cortical neuron. Furthermore, at particular combinations of inputs to thalamocortical and thalamic reticular nucleus cells, thalamic cell bursting correlated strongly with recovery of mutual information between thalamic afferents and layer 4 neurons. These studies suggest that the novel mutual information estimator has advantages over previous estimators and that thalamic reticular nucleus activity can enhance mutual information between thalamic afferents and thalamorecipient cells in the cortex. NEW & NOTEWORTHY In this study, a novel mutual information estimator was developed to analyze information flow in a model thalamocortical network. Our findings suggest that this estimator is a suitable tool for signal transmission analysis, particularly in neural circuits with disparate firing rates, and that the thalamic reticular nucleus can potentiate ascending sensory signals, while thalamic recipient cells in the cortex can recover mutual information in ascending sensory signals that is lost due to thalamic bursting.
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Tancredi, Virginia, Giuseppe Biagini, Margherita D'Antuono, Jacques Louvel, René Pumain, and Massimo Avoli. "Spindle-Like Thalamocortical Synchronization in a Rat Brain Slice Preparation." Journal of Neurophysiology 84, no. 2 (August 1, 2000): 1093–97. http://dx.doi.org/10.1152/jn.2000.84.2.1093.
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We obtained rat brain slices (550–650 μm) that contained part of the frontoparietal cortex along with a portion of the thalamic ventrobasal complex (VB) and of the reticular nucleus (RTN). Maintained reciprocal thalamocortical connectivity was demonstrated by VB stimulation, which elicited orthodromic and antidromic responses in the cortex, along with re-entry of thalamocortical firing originating in VB neurons excited by cortical output activity. In addition, orthodromic responses were recorded in VB and RTN following stimuli delivered in the cortex. Spontaneous and stimulus-induced coherent rhythmic oscillations (duration = 0.4–3.5 s; frequency = 9–16 Hz) occurred in cortex, VB, and RTN during application of medium containing low concentrations of the K+ channel blocker 4-aminopyridine (0.5–1 μM). This activity, which resembled electroencephalograph (EEG) spindles recorded in vivo, disappeared in both cortex and thalamus during application of the excitatory amino acid receptor antagonist kynurenic acid in VB ( n = 6). By contrast, cortical application of kynurenic acid ( n = 4) abolished spindle-like oscillations at this site, but not those recorded in VB, where their frequency was higher than under control conditions. Our findings demonstrate the preservation of reciprocally interconnected cortical and thalamic neuron networks that generate thalamocortical spindle-like oscillations in an in vitro rat brain slice. As shown in intact animals, these oscillations originate in the thalamus where they are presumably caused by interactions between RTN and VB neurons. We propose that this preparation may help to analyze thalamocortical synchronization and to understand the physiopathogenesis of absence attacks.
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Smith, Gregory D., Charles L. Cox, S. Murray Sherman, and John Rinzel. "Fourier Analysis of Sinusoidally Driven Thalamocortical Relay Neurons and a Minimal Integrate-and-Fire-or-Burst Model." Journal of Neurophysiology 83, no. 1 (January 1, 2000): 588–610. http://dx.doi.org/10.1152/jn.2000.83.1.588.
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We performed intracellular recordings of relay neurons from the lateral geniculate nucleus of a cat thalamic slice preparation. We measured responses during both tonic and burst firing modes to sinusoidal current injection and performed Fourier analysis on these responses. For comparison, we constructed a minimal “integrate-and-fire-or-burst” (IFB) neuron model that reproduces salient features of the relay cell responses. The IFB model is constrained to quantitatively fit our Fourier analysis of experimental relay neuron responses, including: the temporal tuning of the response in both tonic and burst modes, including a finding of low-pass and sometimes broadband behavior of tonic firing and band-pass characteristics during bursting, and the generally greater linearity of tonic compared with burst responses at low frequencies. In tonic mode, both experimental and theoretical responses display a frequency-dependent transition from massively superharmonic spiking to phase-locked superharmonic spiking near 3 Hz, followed by phase-locked subharmonic spiking at higher frequencies. Subharmonic and superharmonic burst responses also were observed experimentally. Characterizing the response properties of the “tuned” IFB model leads to insights regarding the observed stimulus dependence of burst versus tonic response mode in relay neurons. Furthermore the simplicity of the IFB model makes it a candidate for large scale network simulations of thalamic functioning.
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Cox, C. L., J. R. Huguenard, and D. A. Prince. "Cholecystokinin depolarizes rat thalamic reticular neurons by suppressing a K+ conductance." Journal of Neurophysiology 74, no. 3 (September 1, 1995): 990–1000. http://dx.doi.org/10.1152/jn.1995.74.3.990.
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1. The thalamic reticular nucleus (nRt) is innervated by cholecystokinin (CCK)-containing neurons and contains CCK binding sites. We used tight-seal, whole cell recording techniques with in vitro rat thalamic slices to investigate the action of CCK on neurons in nRt and ventrobasal thalamus (VB). 2. Brief applications of the CCK agonist cholecystokinin octapeptide (26-33) sulfated (CCK8S) evoked prolonged spike discharges in nRt neurons but had no direct effects on VB neuron activity. This selective excitatory action of CCK8S in nRt resulted from a long-lasting membrane depolarization (2-10 min) associated with an increased input resistance. Voltage-clamp recordings revealed that CCK8S reduced membrane conductance by 0.6-3.8 nS, which amounted to 5-54% of the resting conductance of these neurons. 3. The conductance blocked by CCK8S was linear over the range of -50 to -100 mV and reversed near the potassium equilibrium potential. Modifications of extracellular K+ concentration altered the reversal potential of the conductance as predicted by the Nernst equation. The K+ channel blocker Cs+, applied either intracellularly or combined intra- and extracellularly, blocked the response to CCK8S. 4. The CCK8S-induced depolarization persisted after suppression of synaptic transmission by either tetrodotoxin or a low-Ca2+, high-Mg2+ extracellular solution, indicating that the depolarization was primarily due to activation of postsynaptic CCK receptors and not mediated through the release of other neurotransmitters. 5. The selective CCKA antagonists L364,718 and Cam-1481 attenuated the CCK8S-induced depolarization, whereas the CCKB antagonist L365,260 had little or no effect on the depolarization. 6. Our findings indicate that CCK8S, acting via CCKA-type receptors, reduces a K+ leak current, resulting in a long-lasting membrane depolarization that can presumably modify the firing mode of nRt neurons. Through this effect, CCK actions in nRt may strongly influence thalamocortical function.
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Nielsen, Rune Damgaard, Maja Abitz, and Bente Pakkenberg. "NEURON AND GLIAL CELL NUMBERS IN THE MEDIODORSAL THALAMIC NUCLEUS IN BRAINS OF SCHIZOPHRENIC SUBJECTS." Image Analysis & Stereology 27, no. 3 (May 3, 2011): 133. http://dx.doi.org/10.5566/ias.v27.p133-141.
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Several stereological studies of schizophrenic subjects have shown reduction in both the total number of neurons and in the total volume of the mediodorsal thalamic nucleus (MD). This is in contrast to other studies in that no differences have been found. Using systematic random sampling and an optical fractionator design, the total number of neuron and glial cells in the MD subdivisions: parvocellular (MDPC), magnocellular (MDMC), and densocellular (MDDC) were counted in brains from 9 schizophrenic and 8 control subjects. The control subjects were age, height and body-weight matched to the schizophrenic subjects. We found the neuronal numbers in the schizophrenic subjects to range more than a factor of two, from 3.68 to 9.22 x 106. This is in contrast to the control subjects, who ranged from 5.24 to 7.10 x 106 in neuronal cell numbers. Within our inhomogeneous sample, some schizophrenic subjects thus exhibited relative high total neuron numbers in MD, while others exhibited relative low neuron numbers. The result is in line with the heterogeneity of this severe mental disease and may help to explain why different research groups get different results. The major limitation in this study is the small number of brains of schizophrenic subjects with a high degree of inhomogeneity in length of disease and age of onset. The debates of the comparison of the neurons in the MD in brains of schizophrenic subjects and control subjects and the possible impact of this variance on the disease are still not complete.
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Douglas, Rodney J., Kevan A. C. Martin, and David Whitteridge. "A Canonical Microcircuit for Neocortex." Neural Computation 1, no. 4 (December 1989): 480–88. http://dx.doi.org/10.1162/neco.1989.1.4.480.
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We have used microanatomy derived from single neurons, and in vivo intracellular recordings to develop a simplified circuit of the visual cortex. The circuit explains the intracellular responses to pulse stimulation in terms of the interactions between three basic populations of neurons, and reveals the following features of cortical processing that are important to computational theories of neocortex. First, inhibition and excitation are not separable events. Activation of the cortex inevitably sets in motion a sequence of excitation and inhibition in every neuron. Second, the thalamic input does not provide the major excitation arriving at any neuron. Instead the intracortical excitatory connections provide most of the excitation. Third, the time evolution of excitation and inhibition is far longer than the synaptic delays of the circuits involved. This means that cortical processing cannot rely on precise timing between individual synaptic inputs.
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Shosaku, A. "Cross-correlation analysis of a recurrent inhibitory circuit in the rat thalamus." Journal of Neurophysiology 55, no. 5 (May 1, 1986): 1030–43. http://dx.doi.org/10.1152/jn.1986.55.5.1030.
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Spontaneous activities of vibrissa-responding neurons in the rat ventrobasal complex (VB) and somatosensory part of the thalamic reticular nucleus (S-TR) were simultaneously recorded and subjected to cross-correlation analysis to investigate the functional organization of recurrent inhibitory action of the S-TR on VB neurons. Excitatory and/or inhibitory interactions were found between approximately 75% (25/34) of the pairs of S-TR and VB neurons with receptive fields (RFs) on the same vibrissa. In contrast, there was no significant interaction between 54 pairs of neurons having RFs on different vibrissae. Among the pairs of neurons with RFs on the same vibrissa, there were four types of correlations, which indicate the following connections: monosynaptic excitation from a VB to an S-TR neuron (7 pairs), monosynaptic inhibition from an S-TR to a VB neuron (10 pairs), reciprocal connection combining the above two types (7 pairs), and common excitation in addition to inhibition from an S-TR to a VB neuron (1 pair). Examples of divergence and convergence of connections between S-TR and VB neurons were demonstrated by testing one S-TR (VB) neuron with more than one VB (S-TR) neuron. Vibrissa-suppressed VB cells, which had exclusively inhibitory RFs, were included in eight pairs of the above samples. These VB cells were more likely to receive inhibitory inputs from S-TR neurons than other VB neurons. Cells with RFs on multiple vibrissae were included in the other 10 pairs. These multiple-vibrissa cells had no interaction with single-vibrissa cells but did with multiple-vibrissa cells. From the incidence of four types of correlation between S-TR and VB neurons with RFs on the same vibrissa, the following connection pattern is suggested: One S-TR neuron receives excitatory inputs from approximately 40% of the VB neurons with RFs on the same vibrissa and sends inhibitory outputs to approximately 55%. Since these two groups of VB neurons were overlapping, the S-TR neuron has reciprocal connections with approximately 20% of the VB neurons with RFs on the same vibrissa. The same estimate was applied to connectivity of one VB neuron. These results indicate that both inputs and outputs of S-TR neurons are precisely and topographically organized, although there is convergence to and divergence from a substantial number of VB neurons with RFs on the same vibrissa. It is proposed that the recurrent inhibitory circuit through the S-TR plays a role in improving discrimination of sensory information transmitted through the VB.
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Lytton, William W., and Terrence J. Sejnowski. "Computer model of ethosuximide's effect on a thalamic neuron." Annals of Neurology 32, no. 2 (August 1992): 131–39. http://dx.doi.org/10.1002/ana.410320204.
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Devia, Christ, Manuel A. Duarte-Mermoud, and María de la Luz Aylwin O. "Knowledge-Based Expert Control of Thalamic Neuron Firing Mode." Asian Journal of Control 16, no. 1 (September 27, 2012): 117–25. http://dx.doi.org/10.1002/asjc.599.
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Swadlow, Harvey A., and Alexander G. Gusev. "The Influence of Single VB Thalamocortical Impulses on Barrel Columns of Rabbit Somatosensory Cortex." Journal of Neurophysiology 83, no. 5 (May 1, 2000): 2802–13. http://dx.doi.org/10.1152/jn.2000.83.5.2802.
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Extracellular recordings were obtained from single neurons in ventrobasal (VB) thalamus of awake rabbits while field potentials were recorded at various depths within topographically aligned and nonaligned barrel columns of somatosensory cortex (S1). Spike-triggered averages of cortical field potentials were obtained following action potentials in thalamic neurons. Action potentials in a VB neuron elicited a cortical response within layer 4 with three distinct components. 1) A biphasic, initially positive response (latency <1 ms) was interpreted to reflect activation of the VB axon terminals (the AxTP). This response was not affected by infusion of an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist within the barrel. In contrast, later components of the response were completely eliminated and were interpreted to reflect focal synaptic potentials. 2) A negative potential [focal synaptic negativity (FSN)] occurred at a mean latency of 1.65 ms and lasted ∼4 ms. This response had a rapid rise time (∼0.7 ms) and was interpreted to reflect monosynaptic excitation. 3) The third component was a positive potential (the FSP), with a slow rise time and a half-amplitude duration of ∼30 ms. The FSP showed a weak reversal in superficial cortical layers and was interpreted to reflect di/polysynaptic inhibition. The amplitudes of the AxTP, the FSN, and the FSP reached a peak near layer 4 and were highly attenuated in both superficial and deep cortical layers. All components were attenuated or absent when the cortical electrode was missaligned from the thalamic electrode by a single cortical barrel. Deconvolution procedures revealed that the autocorrelogram of the presynaptic VB neuron had very little influence on either the amplitude or duration of the AxTP or the FSN, and only a minor influence (mean, 11%) on the amplitude of the FSP. We conclude that individual VB thalamic impulses entering a cortical barrel engage both monosynaptic excitatory and di/polysynaptic inhibitory mechanisms. Putative inhibitory interneurons of an S1 barrel receive a highly divergent/convergent monosynaptic input from the topographically aligned VB barreloid, and this results in sharp synchrony among these interneurons. We suggest that single-fiber access to disynaptic inhibition is facilitated by this sharp synchrony, and that the FSP reflects a consequent synchronous wave of feed-forward inhibition within the S1 barrel.
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Morin, L. R., and J. H. Blanchard. "Neuropeptide Y and enkephalin immunoreactivity in retinorecipient nuclei of the hamster pretectum and thalamus." Visual Neuroscience 14, no. 4 (July 1997): 765–77. http://dx.doi.org/10.1017/s0952523800012712.
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AbstractThis investigation was stimulated by the historical confusion concerning the identity of certain pretectal nuclei and by large differences reported between species with respect to which nuclei receive retinal innervation. Subcortical visual nuclei were studied using immunohistochemistry to identify retinal projections labeled following intraocular injection of cholera toxin, b fragment. In addition, neuropeptide Y (NPY) or enkephalin (ENK) immunoreactive cells and fibers were also evaluated in the retinorecipient pretectal and thalamic areas. The results confirm the established view that the retina directly innervates the nucleus of the optic tract (NOT), posterior (PPT) and olivary pretectal (OPT) nuclei. However, the retina also innervates the hamster medial (MPT) and anterior (APT; dorsal division) pretectal nuclei, results not previously reported in rodents. A commissural pretectal area (CPT) sparsely innervated by retina is also described. The data show for the first time that the posterior limitans nucleus (PLi) receives a moderately dense, direct retinal input. The PLi does not project to the cortex and appears to be a pretectal, rather than thalamic, nucleus. All retinal projections are bilateral, although predominantly contralateral The PLi contains a moderately dense plexus of NPY- and ENK-IR fibers and terminals. However, peptidergic fibes also traverse the APT and connect with the dorsomedial pretectum. The OPT contains ENK- and NPY-IR neurons and fibers, but is specifically identifiable by a moderately dense plexus of ENK-IR terminals. Numerous ENK-IR neurons are found in the NOT and PPT. The latter also has moderate numbers of ENK-IR fibers and terminals b few NPY-IR neurons or fibers. The MPT contains modest numbers of ENK-IR fibers. The APT has no NPY-IR neurons or terminals, but an occasional ENK-IR neuron is seen and there is sparse ENK-IR innervation Peptidergic innervation of the visual nuclei does not appear to be derived from the retina. The results show a set of retinally innervated, contiguous nuclei extending from the thalamic ventrolateral geniculate nucleus dorsomedially to the midbrain CPT. These nuclei plus the superior colliculus comprise a dorsal “visual shell” embracing a central core of caudal thalamus and rostral midbrain.
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Sohal, Vikaas S., Charles L. Cox, and John R. Huguenard. "Localization of CCK Receptors in Thalamic Reticular Neurons: A Modeling Study." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2820–24. http://dx.doi.org/10.1152/jn.1998.79.5.2820.
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Sohal, Vikaas S., Charles L. Cox, and John R. Huguenard. Localization of CCK receptors in thalamic reticular neurons: a modeling study. J. Neurophysiol. 79: 2827–2831, 1998. In an earlier experimental study, intracellular recording suggested that cholecystokinin (CCK) suppresses a K+ conductance in thalamic reticular (RE) neurons, yet the reversal potential of the CCK response, revealed using voltage clamp, was hyperpolarized significantly relative to the K+ equilibrium potential. Here, biophysical models of RE neurons were developed and used to test whether suppression of the K+ conductance, g K, can account for the CCK response observed in vitro and also to determine the likely site of CCK receptors on RE neurons. Suppression of g K in model RE neurons can reproduce the relatively hyperpolarized reversal potential of CCK responses found using voltage clamp if the voltage clamp becomes less effective at hyperpolarized potentials. Three factors would reduce voltage-clamp effectiveness in this model: the nonnegligible series resistance of the voltage-clamp electrode, a hyperpolarization-activated mixed cation current ( I h) in RE neurons, and the dendritic location of CCK-sensitive K+ channels. Although suppression of g K in the dendritic compartments of model RE neurons simulates both the magnitude and reversal potential of the CCK response, suppression of g K in just the somatic compartment of model RE neurons fails to do so. Thus the model predicts that CCK should effectively suppress K+ conductance RE neuron dendrites and thereby regulate burst firing in RE neurons. This may explain the potent effects of CCK on intrathalamic oscillations in vitro.
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Tanibuchi, Ikuo, and Patricia S. Goldman-Rakic. "Dissociation of Spatial-, Object-, and Sound-Coding Neurons in the Mediodorsal Nucleus of the Primate Thalamus." Journal of Neurophysiology 89, no. 2 (February 1, 2003): 1067–77. http://dx.doi.org/10.1152/jn.00207.2002.
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The mediodorsal nucleus (MD) is the thalamic gateway to the prefrontal cortex, an area of the brain associated with spatial and object working memory functions. We have recorded single-neuron activities from the MD nucleus in monkeys trained to perform spatial tasks with peripheral visual stimuli and a nonspatial task with foveally presented pictures of objects and faces—tasks identical to those we have previously used to map regional specializations in the dorso- and ventro-lateral prefrontal cortex, respectively. We found that MD neurons exhibited categorical specificity—either responding selectively to locations in the spatial tasks or preferentially to specific representations of faces and objects in the nonspatial task. Spatially tuned neurons were located in parts of the MD connected with the dorsolateral prefrontal cortex while neurons responding to the identity of stimuli mainly occupied more ventral positions in the nucleus that has its connections with the inferior prefrontal convexity. Neuronal responses to auditory stimuli were also examined, and vocalization sensitive neurons were found in more posterior portions of the MD. We conclude that MD neurons are dissociable by their spatial and nonspatial coding properties in line with their cortical connections and that the principle of information segregation in cortico-cortical pathways extends to the “association” nuclei of the thalamus.
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Pritchard, T. C., R. B. Hamilton, and R. Norgren. "Neural coding of gustatory information in the thalamus of Macaca mulatta." Journal of Neurophysiology 61, no. 1 (January 1, 1989): 1–14. http://dx.doi.org/10.1152/jn.1989.61.1.1.
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1. Extracellular action potentials were recorded from single neurons in the parvicellular division of the ventroposteromedial (VPMpc) nucleus of the thalamus of restrained, but alert, Old World monkeys during gustatory, tactile, and thermal stimulation of the oral cavity. In contrast to previous reports in anesthetized or paralyzed rats, the spontaneous activity of these neurons was brisk and their evoked responses robust. 2. Each of 50 taste-responsive neurons was tested with 1.0 M sucrose, 0.1 M NaCl, 0.003 M HCl, and 0.001 M QHCl before other concentrations of the same stimuli were used. Sucrose, which was effective in 80% of the neurons tested, evoked the largest responses of the 4 standard gustatory stimuli (16.1 spikes/s). The average response to NaCl, an effective stimulus for 44% of the neurons in the sample, was 7.5 spikes/s. HCl and QHCl, which few neurons responded to, typically evoked smaller responses. 3. Most of the neurons tested showed monotonic intensity-response (I-R) functions. The power functions showed about the same degree of compression (range = 0.39-0.53), which has been described previously for brain stem neurons in anesthetized rodents. Only 9.1% of the responses were inhibitory, and there was no tendency for these responses to be associated with either specific neurons or stimuli. These data suggest that quality coding of gustatory information in the thalamus is not radically different from that seen among lower-order neurons in other species. 4. Through the use of hierarchical cluster analysis, it was possible to divide the neuron sample into 2 groups, one of which consisted of sucrose-best neurons that had an average entropy value of 0.56. The neurons in the other group, though more heterogeneous, showed either primary or side-band sensitivity to NaCl. The average breadth of responsiveness of the 50 thalamic neurons as described by the entropy coefficient was 0.73. 5. In addition to gustatory neurons, tactile (n = 15), thermal (n = 1), and nonresponsive (n = 25) neurons also were located within VPMpc. An additional 48 neurons that could not be classified as either sensory or motor in nature, inhibited their bursting spontaneous discharge just prior to the onset of fluid stimulation. Only 2 of these neurons demonstrated differential chemical sensitivity. The presence of these nongustatory neurons within the thalamic taste area suggests that the traditional characterization of VPMpc as a gustatory relay may understate its role in ingestive behavior and ignore other noningestive functions of the area.
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McDevitt, Dillon S., and Nicholas M. Graziane. "Timing of Morphine Administration Differentially Alters Paraventricular Thalamic Neuron Activity." eneuro 6, no. 6 (November 2019): ENEURO.0377–19.2019. http://dx.doi.org/10.1523/eneuro.0377-19.2019.
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Ohya, Atsushi, Masayoshi Tsuruoka, Eiichi Imai, Hideki Fukunaga, Akiyuki Shinya, Ryoichi Furuya, Tadaharu Kawawa, and Yoichiro Matsui. "Thalamic- and cerebellar-projecting interpolaris neuron responses to afferent inputs." Brain Research Bulletin 32, no. 6 (January 1993): 615–21. http://dx.doi.org/10.1016/0361-9230(93)90163-6.
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