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Neurochemical studies on the role of glycine as a neurotransmitter in rat brain

Neurochemical studies on the role of glycine as a neurotransmitter in rat brain
Neurochemical studies on the role of glycine as a neurotransmitter in rat brain

During the last two decades it has beocme widely accepted that L-glutamate and L-aspartate are the primary enodgenous excitatory neurotransmitters. Conversely, γ-aminobutyric acid (GABA) and glycine are the inhibitory neurotransmitters in the mammalian CNS. The excitatory neurotransmitters mediate their excitatory actions through at least four different receptor classes, viz. N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, and the metabotropic recetpors. Since the discovery that glycine augmented NMDA actions (Johnson & Ascher 1987), attempts have been made to evaluate its role in several neuropathological states, for example, hypoxia/ischaemia, epilepsy and CNS trauma, which are believed to involve abnormal stimulation of NMDA receptors.

It is therefore possible that glycine may serve as a co-transmitter/allosteric regulator of NMGDA receptor function in the CNS. Parameters affecting the uptake of [3H]glycine into synaptosomes prepared from rat forebrain and striatum were investigated in a sodium-containing medium. [3H]Glycine and [3H]glutamate uptake were found to be Na+ , time and concentration dependent. [3H]Glycine uptake, into different regions of the CNS and different fractions of crude synaptosomes was varied. A variety of compounds was investigated for their ability to influence [3H]glycine uptake. The presence of L-alanine decreased [3H]glycine uptake up by 40%. In experiments to investigate the cellular localization of the uptake sites, it was found that the uptake of [3H]glycine and [3H]glutamate into striatal homogenates was significantly decreased by 28% and 23.3% respectively, two weeks following lesioning of the frontal cortical region to destroy the cortico-striatal glutamatergic fibres. The striatal injection of 120 nmol of the excitotoxin quinolinic acid two weeks previously, led to a significant reduction in both [3H]glycine and [3H]glutamate uptake into striatal homogenates.

University of Southampton
Tawati, Ahmed Mohamed
Tawati, Ahmed Mohamed

Tawati, Ahmed Mohamed (1994) Neurochemical studies on the role of glycine as a neurotransmitter in rat brain. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

During the last two decades it has beocme widely accepted that L-glutamate and L-aspartate are the primary enodgenous excitatory neurotransmitters. Conversely, γ-aminobutyric acid (GABA) and glycine are the inhibitory neurotransmitters in the mammalian CNS. The excitatory neurotransmitters mediate their excitatory actions through at least four different receptor classes, viz. N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, and the metabotropic recetpors. Since the discovery that glycine augmented NMDA actions (Johnson & Ascher 1987), attempts have been made to evaluate its role in several neuropathological states, for example, hypoxia/ischaemia, epilepsy and CNS trauma, which are believed to involve abnormal stimulation of NMDA receptors.

It is therefore possible that glycine may serve as a co-transmitter/allosteric regulator of NMGDA receptor function in the CNS. Parameters affecting the uptake of [3H]glycine into synaptosomes prepared from rat forebrain and striatum were investigated in a sodium-containing medium. [3H]Glycine and [3H]glutamate uptake were found to be Na+ , time and concentration dependent. [3H]Glycine uptake, into different regions of the CNS and different fractions of crude synaptosomes was varied. A variety of compounds was investigated for their ability to influence [3H]glycine uptake. The presence of L-alanine decreased [3H]glycine uptake up by 40%. In experiments to investigate the cellular localization of the uptake sites, it was found that the uptake of [3H]glycine and [3H]glutamate into striatal homogenates was significantly decreased by 28% and 23.3% respectively, two weeks following lesioning of the frontal cortical region to destroy the cortico-striatal glutamatergic fibres. The striatal injection of 120 nmol of the excitotoxin quinolinic acid two weeks previously, led to a significant reduction in both [3H]glycine and [3H]glutamate uptake into striatal homogenates.

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Published date: 1994

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Local EPrints ID: 462612
URI: http://eprints.soton.ac.uk/id/eprint/462612
PURE UUID: abaa383f-8ce9-4c47-9bf1-dec91142a86e

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Date deposited: 04 Jul 2022 19:31
Last modified: 04 Jul 2022 19:31

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Author: Ahmed Mohamed Tawati

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