Presynaptic excitability as a potential target for the treatment of the traumatic cerebellum

Document Type

Article

Abstract

Using an extracellular recording method, we have previously shown a hyperexcitability of the presynaptic response in fluid percussion injury (FPI) in rats. In this study, we demonstrated that treatment with cis-ACBD, a glutamate reuptake inhibitor, depressed the presynaptic potential (PSP) in naive/sham controls, while it potentiated the PSP in FPI rats. On the contrary, (RS)-APICA, a selective group II metabotropic glutamate receptor antagonist, potentiated PSP in controls, but depressed PSP in FPI rats. These results indicate that an alteration of the normal function of metabotropic glutamate receptors and glutamate reuptake system or an altered reactivity of presynaptic fibers was induced by FPI. This alteration may contribute to the reported loss of Purkinje cells after FPI. PSP may be used as a potential tool for evaluating treatments of FPI or as a potential target for the prevention of Purkinje cell death. Copyright © 2004 S. Karger AG, Basel.

Keywords

Cerebellum, Experimental treatment, Neurotransmission, Presynaptic excitability, Purkinje cell death, Traumatic brain injury, Traumatic cerebellum

Publication Date

8-26-2004

Publication Title

Pharmacology

ISSN

00317012

Volume

71

Issue

4

First Page

192

Last Page

198

PubMed ID

15240995

Digital Object Identifier (DOI)

10.1159/000078085

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