Striatal glutamatergic function: modifications following specific lesions.
Brain Res
; 235(1): 83-91, 1982 Mar 04.
Article
em En
| MEDLINE
| ID: mdl-6145487
ABSTRACT
The effects of specific lesions of the striatum (a) hemidecortication; (b) striatal injection of (+/-) ibotenate; and (c) 6-hydroxydopamine injections into the substantia nigra, were investigated on specific [3H]glutamate binding to striatal membranes. One month after decortication, there was a substantial reduction of calcium-dependent, stimulated glutamate release from striatal slices, indicating effective loss of glutamatergic fibres. Striatal glutamate binding increased by approximately 30% and this supersensitivity could be attributed solely to an increased receptor density. Ibotenate lesions which destroy target neurones for the glutamatergic fibres (sparing terminals), reduced glutamate binding in the striatum, as did nigral 6-OHDA lesions which delete striatal dopaminergic terminals. This finding supports the concept of there being glutamate receptors on pre-synaptic dopamine terminals in the striatum, involved in regulation of dopamine release. 6-OHDA lesions also result in a supersensitivity of the dopamine receptors localized on the cortico-striatal afferent terminals, as evidenced by the enhanced ability of dopamine to inhibit the K+-evoked, calcium-dependent release of endogenous striatal glutamate.
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Base de dados:
MEDLINE
Assunto principal:
Corpo Estriado
/
Glutamatos
Limite:
Animals
Idioma:
En
Revista:
Brain Res
Ano de publicação:
1982
Tipo de documento:
Article