Corticosterone disrupts glucose-, but not lactate-supported hippocampal PS-LTP

Abstract

We previously reported that acute exposure of rat hippocampal brain slices to stress levels of corticosterone aggravated ischemic neuronal damage. The present study examined whether or not an acute stress level corticosterone exposure interferes with expression of rat hippocampal CA1 population spike long-term potentiation (PS-LTP) in slices supplemented either with glucose or lactate. Exposure of glucose-supplemented (5mM) slices to corticosterone (1microM) for 90min significantly diminished their ability to generate and maintain PS-LTP compared to equicaloric lactate-supplemented (10mM) slices (p<0.05). Moreover, this diminished expression of LTP in glucose-supplemented slices was ameliorated by either treatment with RU38486 (5microM), a potent corticosterone receptor antagonist or with10mM glucose. These results suggest that lactate may serve as an effective alternate energy substrate during exposure to elevated levels of corticosterone, allowing maintenance of glucocorticoid-sensitive neuronal functions such as synaptic potentiation during metabolically critical periods when glucose utilization is compromised.