The Experts below are selected from a list of 19164 Experts worldwide ranked by ideXlab platform
Terrence J Sejnowski - One of the best experts on this subject based on the ideXlab platform.
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self sustained rhythmic activity in the thalamic reticular nucleus mediated by depolarizing gaba a receptor potentials
Nature Neuroscience, 1999Co-Authors: Maxim Bazhenov, Igor Timofeev, Mircea Steriade, Terrence J SejnowskiAbstract:Intracellular recordings from reticular thalamic (RE) neurons in vivo revealed inhibitory postsynaptic potentials (IPSPs) between RE cells that reversed and became depolarizing at the hyperpolarized membrane potentials that occur during sleep. These excitatory IPSPs can directly trigger Low-Threshold Spikes (LTSs). The oscillatory mechanisms underlying IPSP-triggered LTSs crowned by spike bursts were investigated in models of isolated RE networks. In a one-dimensional network model, external stimulation evoked waves of excitation propagating at a constant velocity of 25‐150 cells per second. In a large-scale, two-dimensional model of the reticular nucleus, the network showed transient or self-sustained oscillations controlled by the maximum conductance of the Low-Threshold calcium current and the membrane potential. This model predicts that the isolated reticular nucleus could initiate sequences of spindle oscillations in thalamocortical networks in vivo.
Heesup Shin - One of the best experts on this subject based on the ideXlab platform.
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t type channels control the opioidergic descending analgesia at the low threshold spiking gabaergic neurons in the periaqueductal gray
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Cheongdahm Park, Jonghyun Kim, Bo Eun Yoon, Eui Ju Choi, Justin C Lee, Heesup ShinAbstract:Endogenous opioids generate analgesic signals in the periaqueductal gray (PAG). However, because cell types in the PAG are difficult to identify, its neuronal mechanism has remained poorly understood. To address this issue, we characterized PAG neurons by their electrical properties using differentially labeled GABAergic and output neurons in the PAG. We found that GABAergic neurons were mostly fast-spiking cells and could be further divided into two distinct classes: with or without Low-Threshold Spikes (LTS) driven by T-type channels. In contrast, the PAG output neurons lacked LTS and showed heterogeneous firing patterns. To reveal the function of the LTS, we examined the mutant mice lacking the α1G T-type channels (α1G−/−). The mutant mice lacked LTS in the fast-spiking GABAergic neurons of the PAG and unexpectedly showed impaired opioid-dependent analgesia; a similar phenotype was reproduced in PAG-specific α1G-knockdown mice. Electrophysiological analyses revealed functional expression of μ-opioid receptors in the low threshold-spiking GABAergic neurons. These neurons in the mutant lacking LTS showed markedly enhanced discharge activities, which led to an augmented inhibition of output neurons. Furthermore, the impaired analgesia observed in α1G−/− mice was reversed by blocking local GABAA receptors. These results indicate that α1G T-type channels are critical for the opioidergic descending analgesia system in the PAG.
Jonghyun Kim - One of the best experts on this subject based on the ideXlab platform.
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t type channels control the opioidergic descending analgesia at the low threshold spiking gabaergic neurons in the periaqueductal gray
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Cheongdahm Park, Jonghyun Kim, Bo Eun Yoon, Eui Ju Choi, Justin C Lee, Heesup ShinAbstract:Endogenous opioids generate analgesic signals in the periaqueductal gray (PAG). However, because cell types in the PAG are difficult to identify, its neuronal mechanism has remained poorly understood. To address this issue, we characterized PAG neurons by their electrical properties using differentially labeled GABAergic and output neurons in the PAG. We found that GABAergic neurons were mostly fast-spiking cells and could be further divided into two distinct classes: with or without Low-Threshold Spikes (LTS) driven by T-type channels. In contrast, the PAG output neurons lacked LTS and showed heterogeneous firing patterns. To reveal the function of the LTS, we examined the mutant mice lacking the α1G T-type channels (α1G−/−). The mutant mice lacked LTS in the fast-spiking GABAergic neurons of the PAG and unexpectedly showed impaired opioid-dependent analgesia; a similar phenotype was reproduced in PAG-specific α1G-knockdown mice. Electrophysiological analyses revealed functional expression of μ-opioid receptors in the low threshold-spiking GABAergic neurons. These neurons in the mutant lacking LTS showed markedly enhanced discharge activities, which led to an augmented inhibition of output neurons. Furthermore, the impaired analgesia observed in α1G−/− mice was reversed by blocking local GABAA receptors. These results indicate that α1G T-type channels are critical for the opioidergic descending analgesia system in the PAG.
Stéphane Dieudonné - One of the best experts on this subject based on the ideXlab platform.
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T-type and L-type Ca2+ conductances define and encode the bimodal firing pattern of vestibulocerebellar unipolar brush cells.
Journal of Neuroscience, 2007Co-Authors: Marco A Diana, Yo Otsu, Gilliane Maton, Thibault Collin, Mireille Chat, Stéphane DieudonnéAbstract:Cerebellar unipolar brush cells (UBCs) are glutamatergic interneurons that receive direct input from vestibular afferents in the form of a unique excitatory synapse on their dendritic brush. UBCs constitute independent relay lines for vestibular signals, and their inherent properties most likely determine how vestibular activity is encoded by the cerebellar cortex. We now demonstrate that UBCs are bimodal cells; they can either fire high-frequency bursts of action potentials when stimulated from hyperpolarized potentials or discharge tonically during sustained depolarizations. The two functional states can be triggered by physiological-like activity of the excitatory input and are encoded by distinct Ca2+-signaling systems. By combining complementary strategies, consisting of molecular and electrophysiological analysis and of ultrafast acousto-optical deflector-based two-photon imaging, we unraveled the identity and the subcellular localization of the Ca2+ conductances activating in each mode. Fast inactivating T-type Ca2+ channels produce Low-Threshold Spikes, which trigger the high-frequency bursts and generate powerful Ca2+ transients in the brush and, to a much lesser extent, in the soma. The tonic firing mode is encoded by a signalization system principally composed of L-type channels. Ca2+ influx during tonic firing produces a linear representation of the spike rate of the cell in the form of a widespread and sustained Ca2+ concentration increase and regulates cellular excitability via BK potassium channels. The bimodal firing pattern of UBCs may underlie different coding strategies of the vestibular input by the cerebellum, thus likely increasing the computational power of this structure.
Cheongdahm Park - One of the best experts on this subject based on the ideXlab platform.
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t type channels control the opioidergic descending analgesia at the low threshold spiking gabaergic neurons in the periaqueductal gray
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Cheongdahm Park, Jonghyun Kim, Bo Eun Yoon, Eui Ju Choi, Justin C Lee, Heesup ShinAbstract:Endogenous opioids generate analgesic signals in the periaqueductal gray (PAG). However, because cell types in the PAG are difficult to identify, its neuronal mechanism has remained poorly understood. To address this issue, we characterized PAG neurons by their electrical properties using differentially labeled GABAergic and output neurons in the PAG. We found that GABAergic neurons were mostly fast-spiking cells and could be further divided into two distinct classes: with or without Low-Threshold Spikes (LTS) driven by T-type channels. In contrast, the PAG output neurons lacked LTS and showed heterogeneous firing patterns. To reveal the function of the LTS, we examined the mutant mice lacking the α1G T-type channels (α1G−/−). The mutant mice lacked LTS in the fast-spiking GABAergic neurons of the PAG and unexpectedly showed impaired opioid-dependent analgesia; a similar phenotype was reproduced in PAG-specific α1G-knockdown mice. Electrophysiological analyses revealed functional expression of μ-opioid receptors in the low threshold-spiking GABAergic neurons. These neurons in the mutant lacking LTS showed markedly enhanced discharge activities, which led to an augmented inhibition of output neurons. Furthermore, the impaired analgesia observed in α1G−/− mice was reversed by blocking local GABAA receptors. These results indicate that α1G T-type channels are critical for the opioidergic descending analgesia system in the PAG.
