Abstract
Stroke is the second leading cause of death worldwide; nevertheless, its pathological mechanism still remains unclear. Besides, there is an urgent need to find new effective treatment strategies for patients with stroke. Hypothermia therapy is widely used in clinical as a neuroprotective strategy practice. However, the exact mechanism is not fully understood. In this study, we examined the effects of hypothermia on glial glutamate transport-1 (GLT-1) and the extracellular glutamate concentration ([Glu]e) in cerebral ischemia–reperfusion insult rats. Our results revealed that cerebral brain ischemia–reperfusion caused the decrease of GLT-1 and Bcl-2, the increase of Bax and [Glu]e, and caused neuron loss. On the contrary, head mild hypothermia (HMH) for 2 hours alleviated the abovementioned effects and exerted neuroprotection. In the hypothermia group, pretreatment with dihydrokainate, a functional antagonist of GLT-1 by lateral ventricle injection partly reversed the abovementioned effect of HMH. Our results suggest that HMH could exert a neuroprotective role by maintaining GLT-1 and reducing the excitotoxicity of [Glu]e during ischemia–reperfusion insult in rats.
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
