The release of excitatory amino acid transmitters in the rat central nervous system
The release of excitatory amino acid transmitters in the rat central nervous system
Tissue preparations of the rat striatum and hippocampal formation have been used to study the release of pre-loaded D-[3H] aspartate and endogenous glutamate in vitro by a continuous perfusion technique. In keeping with the proposed transmitter roles for excitatory amino acids in these brain areas, elevated concentrations of potassium (50mM) specifically increased the rates of efflux of both amino acids, in a manner which was strongly calcium-dependent. Destruction of the cortico-striatal pathway, thought to be the major glutamatergic afferent projection to the striatum, decreased the stimulus-evoked release of endogenous glutamate in the striatum by 302, without any alteration in the basal release rate. Intrastriatalt injections with kainic acid had no effect on the release of endogenous glutamate. Dopamine and a number of analogues specifically antagonised the efflux of glutamate induced by 50mM potassium, again without any change in the rate of spontaneous efflux. Evidence indicates that dopamine acts directly through pre-synaptic receptors located on glutamate terminals in the striatum and the inhibition of glutamate release by dopamine does not appear to involve dopamine-sensitive adenylate cyclase. Striatal lesions using 6(0H) dopamine produced a marked supersensitivity of the response to dopamine, whereas ibotenate lesions were ineffective. Other transmitters, including GABA, 5-HT and acetylcholine, did not alter striatal glutamate release. L-glutamate, and a number of structural analogues inhibited the potassium-stimulated release of both pre-loaded D-[3H] aspartate and endogenous glutamate from the hippocampal formation in vitro. This effect was abolished by selective amino acid antagonists, and, being tetrodotoxin (TTX) insensitive, it was concluded-that the inhibition of glutamate release in the hippocampal formation was probably mediated by presynaptic autoreceptors.
University of Southampton
1981
McBean, Gethin Jane
(1981)
The release of excitatory amino acid transmitters in the rat central nervous system.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Tissue preparations of the rat striatum and hippocampal formation have been used to study the release of pre-loaded D-[3H] aspartate and endogenous glutamate in vitro by a continuous perfusion technique. In keeping with the proposed transmitter roles for excitatory amino acids in these brain areas, elevated concentrations of potassium (50mM) specifically increased the rates of efflux of both amino acids, in a manner which was strongly calcium-dependent. Destruction of the cortico-striatal pathway, thought to be the major glutamatergic afferent projection to the striatum, decreased the stimulus-evoked release of endogenous glutamate in the striatum by 302, without any alteration in the basal release rate. Intrastriatalt injections with kainic acid had no effect on the release of endogenous glutamate. Dopamine and a number of analogues specifically antagonised the efflux of glutamate induced by 50mM potassium, again without any change in the rate of spontaneous efflux. Evidence indicates that dopamine acts directly through pre-synaptic receptors located on glutamate terminals in the striatum and the inhibition of glutamate release by dopamine does not appear to involve dopamine-sensitive adenylate cyclase. Striatal lesions using 6(0H) dopamine produced a marked supersensitivity of the response to dopamine, whereas ibotenate lesions were ineffective. Other transmitters, including GABA, 5-HT and acetylcholine, did not alter striatal glutamate release. L-glutamate, and a number of structural analogues inhibited the potassium-stimulated release of both pre-loaded D-[3H] aspartate and endogenous glutamate from the hippocampal formation in vitro. This effect was abolished by selective amino acid antagonists, and, being tetrodotoxin (TTX) insensitive, it was concluded-that the inhibition of glutamate release in the hippocampal formation was probably mediated by presynaptic autoreceptors.
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Published date: 1981
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Local EPrints ID: 459692
URI: http://eprints.soton.ac.uk/id/eprint/459692
PURE UUID: 4ebfbf9a-eb5e-470f-8752-593a9dd80595
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Date deposited: 04 Jul 2022 17:16
Last modified: 04 Jul 2022 17:16
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Author:
Gethin Jane McBean
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