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Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
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Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
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Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex

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Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex
Journal Article

Effects of a GABAC Receptor Blocker on the Formation of Evoked Potentials in Neuronal Columns in the Rat Somatosensory Cortex

2017
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Overview
Microelectrode studies of the evoked activity of neuronal columns in the barrel cortex in rats showed that the GABAC receptor blocker 1,2,5,6-tetrahydropyridin-4-ylmethylphosphonic acid (TPMPA) had an activatory effect on the secondary components of evoked potentials (EP) mainly of the upper afferent modules of columns as compared with the lower efferent layers. This is evidence that GABAC receptors are located on the presynaptic terminals of thalamocortical glutamatergic afferents and ascending apical dendrites of pyramidal cells. Blockade of GABAC influences with TPMPA led to dose-dependent depolarization of afferents with development of presynaptic inhibition and suppression of the primary responses (PR) of EP. The different effects of the GABAC receptor blocker on the secondary components of EP in the upper layers of the cortex are due to the development of afterhyperpolarization of neurons after high-amplitude PR and afterdepolarization after low-amplitude responses, with subsequent activation of different voltage-gated channels and the formation of different gradients in the direct current (DC) potential of the cortex.