Minimal effect of brain temperature changes on glutamate release in rat following severe global brain ischemia
- 1 December 1998
- journal article
- Published by Wolters Kluwer Health in NeuroReport
- Vol. 9 (17) , 3863-3867
- https://doi.org/10.1097/00001756-199812010-00018
Abstract
USING a dialysis electrode, we recently developed an oxygen-independent system for real-time measurement of the glutamate concentration in the extracellular space ([Glu]e) during ischemia. This system allows separate evaluation of intra-ischemic biphase [Glu]e elevation, i. e. release from synaptic vesicles (1st phase), reversed uptake of glutamate from metabolic pools in neuronal cells (2nd phase), and post-ischemic glutamate re-uptake in ischemia—reperfusion models. Using the system, we attempted to clarify the relationship between biphase glutamate release and brain temperature in a model of acute global ischemia produced by transecting both carotid arteries. Our results showed that, in contrast to mild hyperthermia, hypothermia did not inhibit the 1st phase of [Glu]e release, and changes in intra-ischemic brain temperature had a minimal effect on the 2nd phase of [Glu]e elevation during severe acute ischemia. These findings, together with our previous data, indicate that brain temperature change in the intra-ischemic period plays an important role in disturbance of the glutamate re-uptake system during ischemia. NeuroReport9: 3863–3868 © 1998 Lippincott Williams & Wilkins.Keywords
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