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Eberhard Kochs - One of the best experts on this subject based on the ideXlab platform.
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Contributions of GABAergic and glutamatergic mechanisms to isoflurane-induced suppression of thalamic somatosensory information transfer
Experimental Brain Research, 2007Co-Authors: Christiane Vahle-hinz, Matthias Siemers, Oliver Detsch, Eberhard KochsAbstract:Indications for a pivotal role of the thalamocortical network in producing the state of anesthesia have come from in vivo animal studies as well as imaging studies in humans. We studied possible synaptic mechanisms of anesthesia-induced suppression of touch perception in the rat’s thalamus. Thalamocortical relay neurons (TCNs) receive ascending and descending glutamatergic excitatory inputs via NMDA and non-NMDA receptors (AMPAR) and are subjected to GABA_Aergic inhibitory input which shapes the sensory information conveyed to the cortex. The involvement of these synaptic receptors in the suppressive effects of the prototypic volatile anesthetic isoflurane was assessed by local iontophoretic administration of receptor agonists/antagonists during extracellular recordings of TCNs of the Ventral Posteromedial Nucleus responding to whisker vibration in rats anesthetized with isoflurane concentrations of ∼0.9 vol.% (baseline) and ∼1.9 vol.% ( ISO high ). ISO high induced a profound suppression of response activity reflected by a conversion of the sustained vibratory responses to ON responses. Administration of NMDA, AMPA, or GABA_AR antagonists caused a reversal to sustained responses in 88, 94 and 88% of the neurons, respectively, with a recovery to baseline levels of response activity. The data show that the block of thalamocortical transfer of tactile information under ISO high may result from an enhancement of GABA_Aergic inhibition and/or a reduction of glutamatergic excitation. Furthermore, they show that the ascending vibratory signals still reach the thalamic neurons under the high isoflurane concentration, indicating that this input is resistant to isoflurane while the attenuation of excitation may be brought about at the corticothalamic glutamatergic facilitatory input.
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Differential effects of isoflurane on excitatory and inhibitory synaptic inputs to thalamic neurones in vivo
BJA: British Journal of Anaesthesia, 2002Co-Authors: O. Detsch, Eberhard Kochs, M. Siemers, B. Bromm, C. Vahle-hinzAbstract:Background Mechanosensory thalamocortical relay neurones (TCNs) receive glutamatergic excitatory input and are subjected to γ-aminobutyric acid (GABA)Aergic inhibitory input. This study assessed the effects of an increase in concentration of isoflurane on thalamic excitatory and inhibitory mechanisms. Methods TCNs (n=15) of the thalamic Ventral Posteromedial Nucleus responding to mechanical stimulation of whiskers were investigated in rats anaesthetized with end-tidal concentrations of isoflurane of ∼0.9% (ISOlow, baseline) and ∼1.9% (ISOhigh). Response activity induced by controlled vibratory movement of single whiskers was recorded before, during and after iontophoretic administration of the GABAA receptor antagonist bicuculline to the vicinity of the recorded neurone. Results The increase in concentration of isoflurane induced a suppression of vibratory responses to 14 (4)% [mean ( sem )] of baseline activity. Blockade of GABAA receptors by bicuculline during ISOlow and ISOhigh caused increases in response activity to 259 (32)% and 116 (25)% of baseline activity, respectively. The increase in isoflurane concentration enhanced overall inhibitory inputs by 102 (38)%, whilst overall excitatory inputs were reduced by 54 (7)%. Conclusions These data suggest that doubling the concentration of isoflurane doubles the strength of GABAAergic inhibition and decreases the excitatory drive of TCNs by approximately 50%. The isoflurane-induced enhancement of GABAAergic inhibition led to a blockade of thalamocortical information transfer which was not accomplished by the effects of isoflurane on glutamatergic synaptic transmission alone. Thus, it appears that, with respect to transmission of information in the thalamus, the most prominent action of isoflurane is an enhancement of GABAAergic synaptic inhibition, and that effects on glutamatergic neurotransmission may contribute to a lesser extent.
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Local GABAA receptor blockade reverses isoflurane's suppressive effects on thalamic neurons in vivo
Anesthesia & Analgesia, 2001Co-Authors: Christiane Vahle-hinz, O. Detsch, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline in the thalamic Ventral Posteromedial Nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% ± 0.01%, mean ± sem) were suppressed under large concentrations (1.44% ± 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABAA receptor-mediated inhibition.
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Isoflurane induces dose-dependent changes of thalamic somatosensory information transfer.
Brain Research, 1999Co-Authors: O. Detsch, Christiane Vahle-hinz, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Abstract In spite of several reports about suppressive effects of volatile anesthetics on somatosensation, their neuronal mechanisms are largely unknown. The present study investigates somatosensory impulse transmission at the thalamic level in rats under varied concentrations of isoflurane by recordings of neuronal responses to mechanical stimulation of the body surface. Single-unit recordings of thalamo-cortical relay neurons (TCNs, third order neurons; n =28) and presumed trigemino-thalamic fibers (TTFs, second order neurons; n =7) were performed in the Ventral Posteromedial Nucleus. Functional response characteristics were quantified following defined tactile stimulation (trapezoidal or vibratory deflection of sinus hairs or fur) applied to the neuronal receptive fields. End-tidal isoflurane concentration was increased in steps of 0.2% between 0.6% (baseline) and 2.0%. The response activity in all TCNs studied was suppressed in a dose-dependent manner (2.0% isoflurane decreased responses to 3.5±1.1% of baseline; mean±S.E.M.); the response activity in TTFs was much less affected (decrease to 55.0±8.2%). Suppression of ongoing activity, however, was similar for both, TCNs and TTFs. Furthermore, in TCNs, the response characteristics changed with increasing isoflurane between 1.0% and 1.8%: tonic and sustained responses were converted to phasic on-responses. In contrast, the tonic and sustained response characteristics of TTFs were preserved even at higher isoflurane concentrations. The results indicate that isoflurane attenuates the output of somatosensory signals in the specific Nucleus of the rat's thalamus, while its input is only marginally affected. The observed changes of thalamic neuronal response characteristics, at least in part, may cause the loss in sensory discrimination observed during general anesthesia.
Martin Deschênes - One of the best experts on this subject based on the ideXlab platform.
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Single- and Multi-Whisker Channels in the Ascending Projections from the Principal Trigeminal Nucleus in the Rat
2013Co-Authors: Pierre Veinante, Martin DeschênesAbstract:This study investigated the relationship between axonal projections and receptive field properties of whisker-sensitive cells in the principal trigeminal sensory Nucleus of the rat. The labeling of small groups of trigeminothalamic axons with biotinylated dextran amine disclosed two broad classes of axons; a majority of fibers (68%; n � 107) project to a single barreloid of the Ventral Posteromedial Nucleus, and the remaining group includes axons that innervate both the posterior group of the thalamus and the tectum. Additional terminal sites for axons of this latter group may include the pretectum, the zona incerta, the medial part of the medial geniculate Nucleus, and the Ventral Posteromedial Nucleus. Corresponding to these two classes of fibers, 67 % of the cells in the principal trigeminal Nucleus (n � 313) have single-whisker receptive fields, whereas the rest of the population have receptive fields composed o
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Single- and multi-whisker channels in the ascending projections from the principal trigeminal Nucleus in the rat.
The Journal of Neuroscience, 1999Co-Authors: Pierre Veinante, Martin DeschênesAbstract:This study investigated the relationship between axonal projections and receptive field properties of whisker-sensitive cells in the principal trigeminal sensory Nucleus of the rat. The labeling of small groups of trigeminothalamic axons with biotinylated dextran amine disclosed two broad classes of axons; a majority of fibers (68%; n = 107) project to a single barreloid of the Ventral Posteromedial Nucleus, and the remaining group includes axons that innervate both the posterior group of the thalamus and the tectum. Additional terminal sites for axons of this latter group may include the pretectum, the zona incerta, the medial part of the medial geniculate Nucleus, and the Ventral Posteromedial Nucleus. Corresponding to these two classes of fibers, 67% of the cells in the principal trigeminal Nucleus (n = 313) have single-whisker receptive fields, whereas the rest of the population have receptive fields composed of multiple whiskers. The tonic or phasic properties of the responses apparently bear no relation to the axonal projection patterns. Solid retrograde labeling of cells that project to the Ventral Posteromedial Nucleus and intracellular staining revealed that single-whisker cells have small somata and narrow, barrelette-bounded dendritic trees. In contrast, multi-whisker neurons have large multipolar somata, expansive dendritic trees, and many respond antidromically to stimulation of the superior colliculus. Together, these results provide evidence for two main channels of vibrissal information: a single-whisker channel that links trigeminal barrelettes to their corresponding barreloids, and a multi-whisker channel that distributes principally in the posterior group and tectum.
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intracortical axonal projections of lamina vi cells of the primary somatosensory cortex in the rat a single cell labeling study
The Journal of Neuroscience, 1997Co-Authors: Zhongwei Zhang, Martin DeschênesAbstract:A sample of 84 neurons in lamina VIa of rat somatosensory cortex (S1) was juxtacellularly labeled with biocytin, and the axons of the neurons were traced. Three classes of cells were identified as corticothalamic, corticocortical, and local circuit neurons. Corticothalamic cells (46%) are small, short pyramids projecting either to the Ventral Posteromedial Nucleus alone or to the posterior group as well. The former are in upper lamina VI, have apical dendrites terminating in layer IV, and have intracortical collaterals ascending to layer IV as a narrow column about the size of a barrel. The latter are in the lower half of lamina VI, have apical dendrites terminating in layer V, and have a more extensive network of collaterals terminating in the upper part of lamina V. Corticothalamic cells do not project to distant cortical targets through branching axons. Corticocortical cells (44%) are small, short pyramids, inverted or modified pyramids, or bipolar spiny neurons. They send collaterals principally to infragranular layers of S1 and branches to the second somatosensory cortex, the motor cortex, or the corpus callosum. Local circuit neurons (10%) are basket cells, concentrated in upper lamina VI, having smooth, beaded dendrites and a rich collateral network densely covered with varicosities in layers V and VI. We conclude that (1) dendritic morphology and axonal arborizations of corticothalamic cells relate to the projection target; (2) many apparently diverse layer VI cells project to other cortical fields; and (3) lamina VI is a network for corticothalamic and corticocortical communication.
Christiane Vahle-hinz - One of the best experts on this subject based on the ideXlab platform.
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Contributions of GABAergic and glutamatergic mechanisms to isoflurane-induced suppression of thalamic somatosensory information transfer
Experimental Brain Research, 2007Co-Authors: Christiane Vahle-hinz, Matthias Siemers, Oliver Detsch, Eberhard KochsAbstract:Indications for a pivotal role of the thalamocortical network in producing the state of anesthesia have come from in vivo animal studies as well as imaging studies in humans. We studied possible synaptic mechanisms of anesthesia-induced suppression of touch perception in the rat’s thalamus. Thalamocortical relay neurons (TCNs) receive ascending and descending glutamatergic excitatory inputs via NMDA and non-NMDA receptors (AMPAR) and are subjected to GABA_Aergic inhibitory input which shapes the sensory information conveyed to the cortex. The involvement of these synaptic receptors in the suppressive effects of the prototypic volatile anesthetic isoflurane was assessed by local iontophoretic administration of receptor agonists/antagonists during extracellular recordings of TCNs of the Ventral Posteromedial Nucleus responding to whisker vibration in rats anesthetized with isoflurane concentrations of ∼0.9 vol.% (baseline) and ∼1.9 vol.% ( ISO high ). ISO high induced a profound suppression of response activity reflected by a conversion of the sustained vibratory responses to ON responses. Administration of NMDA, AMPA, or GABA_AR antagonists caused a reversal to sustained responses in 88, 94 and 88% of the neurons, respectively, with a recovery to baseline levels of response activity. The data show that the block of thalamocortical transfer of tactile information under ISO high may result from an enhancement of GABA_Aergic inhibition and/or a reduction of glutamatergic excitation. Furthermore, they show that the ascending vibratory signals still reach the thalamic neurons under the high isoflurane concentration, indicating that this input is resistant to isoflurane while the attenuation of excitation may be brought about at the corticothalamic glutamatergic facilitatory input.
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Local GABAA receptor blockade reverses isoflurane's suppressive effects on thalamic neurons in vivo
Anesthesia & Analgesia, 2001Co-Authors: Christiane Vahle-hinz, O. Detsch, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline in the thalamic Ventral Posteromedial Nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% ± 0.01%, mean ± sem) were suppressed under large concentrations (1.44% ± 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABAA receptor-mediated inhibition.
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Isoflurane induces dose-dependent changes of thalamic somatosensory information transfer.
Brain Research, 1999Co-Authors: O. Detsch, Christiane Vahle-hinz, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Abstract In spite of several reports about suppressive effects of volatile anesthetics on somatosensation, their neuronal mechanisms are largely unknown. The present study investigates somatosensory impulse transmission at the thalamic level in rats under varied concentrations of isoflurane by recordings of neuronal responses to mechanical stimulation of the body surface. Single-unit recordings of thalamo-cortical relay neurons (TCNs, third order neurons; n =28) and presumed trigemino-thalamic fibers (TTFs, second order neurons; n =7) were performed in the Ventral Posteromedial Nucleus. Functional response characteristics were quantified following defined tactile stimulation (trapezoidal or vibratory deflection of sinus hairs or fur) applied to the neuronal receptive fields. End-tidal isoflurane concentration was increased in steps of 0.2% between 0.6% (baseline) and 2.0%. The response activity in all TCNs studied was suppressed in a dose-dependent manner (2.0% isoflurane decreased responses to 3.5±1.1% of baseline; mean±S.E.M.); the response activity in TTFs was much less affected (decrease to 55.0±8.2%). Suppression of ongoing activity, however, was similar for both, TCNs and TTFs. Furthermore, in TCNs, the response characteristics changed with increasing isoflurane between 1.0% and 1.8%: tonic and sustained responses were converted to phasic on-responses. In contrast, the tonic and sustained response characteristics of TTFs were preserved even at higher isoflurane concentrations. The results indicate that isoflurane attenuates the output of somatosensory signals in the specific Nucleus of the rat's thalamus, while its input is only marginally affected. The observed changes of thalamic neuronal response characteristics, at least in part, may cause the loss in sensory discrimination observed during general anesthesia.
Matthias Siemers - One of the best experts on this subject based on the ideXlab platform.
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Contributions of GABAergic and glutamatergic mechanisms to isoflurane-induced suppression of thalamic somatosensory information transfer
Experimental Brain Research, 2007Co-Authors: Christiane Vahle-hinz, Matthias Siemers, Oliver Detsch, Eberhard KochsAbstract:Indications for a pivotal role of the thalamocortical network in producing the state of anesthesia have come from in vivo animal studies as well as imaging studies in humans. We studied possible synaptic mechanisms of anesthesia-induced suppression of touch perception in the rat’s thalamus. Thalamocortical relay neurons (TCNs) receive ascending and descending glutamatergic excitatory inputs via NMDA and non-NMDA receptors (AMPAR) and are subjected to GABA_Aergic inhibitory input which shapes the sensory information conveyed to the cortex. The involvement of these synaptic receptors in the suppressive effects of the prototypic volatile anesthetic isoflurane was assessed by local iontophoretic administration of receptor agonists/antagonists during extracellular recordings of TCNs of the Ventral Posteromedial Nucleus responding to whisker vibration in rats anesthetized with isoflurane concentrations of ∼0.9 vol.% (baseline) and ∼1.9 vol.% ( ISO high ). ISO high induced a profound suppression of response activity reflected by a conversion of the sustained vibratory responses to ON responses. Administration of NMDA, AMPA, or GABA_AR antagonists caused a reversal to sustained responses in 88, 94 and 88% of the neurons, respectively, with a recovery to baseline levels of response activity. The data show that the block of thalamocortical transfer of tactile information under ISO high may result from an enhancement of GABA_Aergic inhibition and/or a reduction of glutamatergic excitation. Furthermore, they show that the ascending vibratory signals still reach the thalamic neurons under the high isoflurane concentration, indicating that this input is resistant to isoflurane while the attenuation of excitation may be brought about at the corticothalamic glutamatergic facilitatory input.
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Local GABAA receptor blockade reverses isoflurane's suppressive effects on thalamic neurons in vivo
Anesthesia & Analgesia, 2001Co-Authors: Christiane Vahle-hinz, O. Detsch, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline in the thalamic Ventral Posteromedial Nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% ± 0.01%, mean ± sem) were suppressed under large concentrations (1.44% ± 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABAA receptor-mediated inhibition.
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Isoflurane induces dose-dependent changes of thalamic somatosensory information transfer.
Brain Research, 1999Co-Authors: O. Detsch, Christiane Vahle-hinz, Matthias Siemers, Eberhard Kochs, Burkhart BrommAbstract:Abstract In spite of several reports about suppressive effects of volatile anesthetics on somatosensation, their neuronal mechanisms are largely unknown. The present study investigates somatosensory impulse transmission at the thalamic level in rats under varied concentrations of isoflurane by recordings of neuronal responses to mechanical stimulation of the body surface. Single-unit recordings of thalamo-cortical relay neurons (TCNs, third order neurons; n =28) and presumed trigemino-thalamic fibers (TTFs, second order neurons; n =7) were performed in the Ventral Posteromedial Nucleus. Functional response characteristics were quantified following defined tactile stimulation (trapezoidal or vibratory deflection of sinus hairs or fur) applied to the neuronal receptive fields. End-tidal isoflurane concentration was increased in steps of 0.2% between 0.6% (baseline) and 2.0%. The response activity in all TCNs studied was suppressed in a dose-dependent manner (2.0% isoflurane decreased responses to 3.5±1.1% of baseline; mean±S.E.M.); the response activity in TTFs was much less affected (decrease to 55.0±8.2%). Suppression of ongoing activity, however, was similar for both, TCNs and TTFs. Furthermore, in TCNs, the response characteristics changed with increasing isoflurane between 1.0% and 1.8%: tonic and sustained responses were converted to phasic on-responses. In contrast, the tonic and sustained response characteristics of TTFs were preserved even at higher isoflurane concentrations. The results indicate that isoflurane attenuates the output of somatosensory signals in the specific Nucleus of the rat's thalamus, while its input is only marginally affected. The observed changes of thalamic neuronal response characteristics, at least in part, may cause the loss in sensory discrimination observed during general anesthesia.
Lin Zhang - One of the best experts on this subject based on the ideXlab platform.
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Ketamine attenuates the glutamatergic neurotransmission in the Ventral Posteromedial Nucleus slices of rats
BMC Anesthesiology, 2017Co-Authors: Chengxi Liu, Yajun Zhang, Lin ZhangAbstract:Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC). Previous studies have demonstrated that thalamocortical system is critical for information transmission and integration in the brain. The Ventral Posteromedial Nucleus (VPM) is a critical component of thalamocortical system. Glutamate is an important excitatory neurotransmitter in the brain and may be involved in ketamine-induced LOC. The study used whole-cell patch-clamp to observe the effect of ketamine (30 μM–1000 μM) on glutamatergic neurotransmission in VPM slices. Ketamine significantly decreased the amplitude of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs), but only higher concentration of ketamine (300 μM and 1000 μM) suppressed the frequency of sEPSCs. Ketamine (100 μM–1000 μM) also decreased the amplitude of glutamatergic miniature excitatory postsynaptic currents (mEPSCs), without altering the frequency. In VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process.
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GABAA Receptor in the Thalamic Specific Relay System Contributes to the Propofol-Induced Somatosensory Cortical Suppression in Rat
PLOS ONE, 2013Co-Authors: Yu Zhang, Chaoping Wang, Yi Zhang, Lin ZhangAbstract:Interaction with the gamma-aminobutyric-acid-type-A (GABAA) receptors is recognized as an important component of the mechanism of propofol, a sedative-hypnotic drug commonly used as anesthetic. However the contribution of GABAA receptors to the central nervous system suppression is still not well understood, especially in the thalamocortical network. In the present study, we investigated if intracerebral injection of bicuculline (a GABAA receptor antagonist) into the thalamus Ventral Posteromedial Nucleus (VPM, a thalamus specific relay nuclei that innervated S1 mostly) could reverse propofol-induced cortical suppression, through recording the changes of both spontaneous and somatosensory neural activities in rat’s somatosensory cortex (S1). We found that after injection of bicuculline into VPM, significant increase of neural activities were observed in all bands of local field potentials (total band, 182±6%), while the amplitude of all components in somatosensory evoked potentials were also increased (negative, 121±9% and positive, 124±6%).These data support that the potentiation of GABAA receptor-mediated synaptic inhibition in a thalamic specific relay system seems to play a crucial role in propofol-induced cortical suppression in the somatosensory cortex of rats.
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Schematic representation of the somatosensory ascending pathway.
2013Co-Authors: Yu Zhang, Chaoping Wang, Yi Zhang, Lin ZhangAbstract:The tactile information was transmitted from mechanoreceptors of the facial skin to the primary somatosensory cortex (S1). The tungsten microelectrode allowed extracellular single-unit recordings in S1, while a glass electrode performed the injection of bicuculline (BIC) in the thalamic Ventral Posteromedial Nucleus (VPM).
