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The electrophysiological and neuropharmacological studies of the ventrolateral thalamus in the rat

The electrophysiological and neuropharmacological studies of the ventrolateral thalamus in the rat
The electrophysiological and neuropharmacological studies of the ventrolateral thalamus in the rat

Adeoshun, 1.0.Electrophysiological and pharmacological studies were made on the thalamocortical relay neurones of the ventro-lateral thalamus in the rat. Experiments were performed on urethane anaesthetizedmale wistar rats of 200 gram weight. The thalamocortical relay cells were identified by two electrophysiological criteria; by stimulating a contralateral hind limb nerve and by the antidromic invasion or thesame cell from the somatosensory cortex. Using those two criteria for identification, the cells were then orthodromically activated fromthe somatosensory cortex. The orthodromically activated principal cells responded to latencies of between 5 and 10 ms with the majority of the cells responding to between 5 to 7.5 ms latency.The neuropharmacological studies involved microiontophoresis of drugs, their agonists and antagonists. Extracellular recordings were made of neuronal responses by using 6-barrelled iontophoretic electrodes with the recording electrode tip protuding 10-20 Jim past the drug barrels.L-glutamate, L-aspartate, DL-aspartate, DL-homocysteate, N-methl-DL-aspartate, Kainate, Ketokainate and acetylcholine were found to excite most cells studied. Gamma-aminobutyric acid was found to be inhibitory and also depressed L-glutamate excitations. Bicuculline was found to block gamma-amino butyric inhibitions.t frAtropine reversibly blocked acetylcholine induced excitation while sparing the amino acids-induced excitations. The relative potencies of a variety of amino acid analogues were also studied. Kainate was found to be most potent followed by Ketokeinate and N-metyl-DL-aspartate relative to L-glutamatc and L-aspartate in terms of iontophoresis. The antagonists, GDEE, D CAA and Atropine were studied on theamino acids induced excitations and acetylcholine. GDEE preferentially depressed L-glutamate, L-aspartate and DL-homocysteate from N-methylDL-aspartate induced excitation. In high concentrations GDEE becomes a non-elective antagonist. D CAA selectively depressed, N-methyl-DL-aspartate, L-aspartate induced excitations and poorly affected L-glutamate and did not affect acetylcholine excitatory responses. Studies of the antagonists were also made on evoked synaptic excitations both from the stimulation of a hind limb nerve and the orthodromic activation from the somatosensory cortex. The synaptic excitation of the principal cell at the ventrolateral thalamus from the cortex is more sensitive to the antagonistic effect of D CAA while the orthodromic activation of the same cell from stimulating the hind limb nerve is more sensitive to GDEE. Atropine did not have any antagonistic effect on both orthodromic activations. In this study it is strongly suggested that L-aspartate is the likely neurotransmitter in the cortico-thalamic pathway.

University of Southampton
Adeoshun, Isaac Olukayode
Adeoshun, Isaac Olukayode

Adeoshun, Isaac Olukayode (1981) The electrophysiological and neuropharmacological studies of the ventrolateral thalamus in the rat. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Adeoshun, 1.0.Electrophysiological and pharmacological studies were made on the thalamocortical relay neurones of the ventro-lateral thalamus in the rat. Experiments were performed on urethane anaesthetizedmale wistar rats of 200 gram weight. The thalamocortical relay cells were identified by two electrophysiological criteria; by stimulating a contralateral hind limb nerve and by the antidromic invasion or thesame cell from the somatosensory cortex. Using those two criteria for identification, the cells were then orthodromically activated fromthe somatosensory cortex. The orthodromically activated principal cells responded to latencies of between 5 and 10 ms with the majority of the cells responding to between 5 to 7.5 ms latency.The neuropharmacological studies involved microiontophoresis of drugs, their agonists and antagonists. Extracellular recordings were made of neuronal responses by using 6-barrelled iontophoretic electrodes with the recording electrode tip protuding 10-20 Jim past the drug barrels.L-glutamate, L-aspartate, DL-aspartate, DL-homocysteate, N-methl-DL-aspartate, Kainate, Ketokainate and acetylcholine were found to excite most cells studied. Gamma-aminobutyric acid was found to be inhibitory and also depressed L-glutamate excitations. Bicuculline was found to block gamma-amino butyric inhibitions.t frAtropine reversibly blocked acetylcholine induced excitation while sparing the amino acids-induced excitations. The relative potencies of a variety of amino acid analogues were also studied. Kainate was found to be most potent followed by Ketokeinate and N-metyl-DL-aspartate relative to L-glutamatc and L-aspartate in terms of iontophoresis. The antagonists, GDEE, D CAA and Atropine were studied on theamino acids induced excitations and acetylcholine. GDEE preferentially depressed L-glutamate, L-aspartate and DL-homocysteate from N-methylDL-aspartate induced excitation. In high concentrations GDEE becomes a non-elective antagonist. D CAA selectively depressed, N-methyl-DL-aspartate, L-aspartate induced excitations and poorly affected L-glutamate and did not affect acetylcholine excitatory responses. Studies of the antagonists were also made on evoked synaptic excitations both from the stimulation of a hind limb nerve and the orthodromic activation from the somatosensory cortex. The synaptic excitation of the principal cell at the ventrolateral thalamus from the cortex is more sensitive to the antagonistic effect of D CAA while the orthodromic activation of the same cell from stimulating the hind limb nerve is more sensitive to GDEE. Atropine did not have any antagonistic effect on both orthodromic activations. In this study it is strongly suggested that L-aspartate is the likely neurotransmitter in the cortico-thalamic pathway.

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Published date: 1981

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Local EPrints ID: 458965
URI: http://eprints.soton.ac.uk/id/eprint/458965
PURE UUID: b7608ecf-07fb-4b77-a6c4-904883fe8ed1

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Date deposited: 04 Jul 2022 17:01
Last modified: 04 Jul 2022 17:01

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Author: Isaac Olukayode Adeoshun

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