Ischemia Increases TREK-2 Channel Expression in Astrocytes: Relevance to Glutamate Clearance

Abstract

The extent of an ischemic insult is less in brain regions enriched in astrocytes suggesting that astrocytes maintain function and buffer glutamate during ischemia. Astrocytes express a wide variety of potassium channels to support their functions including TREK-2 channels which are regulated by polyunsaturated fatty acids, intracellular acidosis and swelling; conditions that pertain to ischemia. The present study investigated the possible involvement of TREK-2 channels in cultured cortical astrocytes during experimental ischemia (anoxia/hypoglycemia) by examining TREK-2 protein levels, channel activity and ability to clear glutamate. We found that TREK-2 protein levels were increased rapidly within 2 hrs of the onset of simulated ischemia. This increase corresponded to an increase in temperature-sensitive TREK-2-like channel conductance and the ability of astrocytes to buffer extracellular glutamate even during ischemia. Together, these data suggest that up-regulation of TREK-2 channels may help rescue astrocyte function and lower extracellular glutamate during ischemia.