Striatal glutamate release is important for development of ischemic damage to striatal neurons during rat heatstroke.

Abstract:

:This study attempted to ascertain whether heatstroke-induced ischemia is associated with augmented striatal glutamate release and can be attenuated by NMDA receptor antagonists. Mean arterial pressure (MAP), striatal cerebral blood flow (CBF), striatal glutamate release and striatal neuronal damage score were assessed in saline-treated rats and in rats treated with NMDA receptor antagonists. Heatstroke was induced by exposing the animals to a high ambient temperature; the moment at which MAP and CBF began to decrease from their peak levels was taken as the onset of heatstroke. During onset of heatstroke, rats displayed higher values of colonic temperature, striatal glutamate release and striatal neuronal damage score, and lower values of MAP and striatal blood flow compared with normothermic control rats. The decreased MAP, the diminished striatal blood flow, the augmented striatal glutamate release and the increased striatal neuronal damage score during onset of heatstroke were significantly attenuated by pretreatment with an NMDA receptor antagonist such as MK-801 or ketamine. In addition, the survival time (interval between onset of heatstroke and death) of the rats was extended by pretreatment with one of these two NMDA receptor antagonists. These results suggest that marked accumulation of glutamate in the striatum is important for the development of ischemic damage to striatal neurons during the onset of heatstroke.

journal_name

Brain Res

journal_title

Brain research

authors

Yang YL,Pan WH,Chiu TH,Lin MT

doi

10.1016/s0006-8993(98)00282-0

subject

Has Abstract

pub_date

1998-06-08 00:00:00

pages

121-7

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

S0006-8993(98)00282-0

journal_volume

795

pub_type

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