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Eur J Neurosci. 1994 Jan 1;6(1):115-20.

Rapid desensitization of the metabotropic glutamate receptor that facilitates glutamate release in rat cerebrocortical nerve terminals.

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  • 1Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, Madrid, Spain.

Abstract

The metabotropic autoreceptor of glutamatergic nerve terminals from the cerebral cortex of adult rats has been characterized. Receptor activation involves a rapid and transient increase in diacylglycerol, which is sensitive to L-2-amino-3-phosphonopropionate (L-AP3) and L-2-amino-4-phosphonobutanoic acid (L-AP4) and is partially blocked by pertussis toxin. Protein kinase C (PKC) has a negative feedback control in this transduction pathway because the activation of the kinase, either by phorbol esters or by the endogenous diacylglycerol produced by the receptor, results in a reversible receptor desensitization, with loss of the ability to further facilitate glutamate release. It is concluded that the facilitatory metabotropic receptor located at the glutamatergic nerve endings belongs to the subclass coupled to phosphoinositide hydrolysis and that the rapid and use-dependent desensitization of the facilitatory pathway may underlie a mechanism to prevent its permanent activation and thereby to avoid neurotoxicity.

PMID:
7907519
[PubMed - indexed for MEDLINE]
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