Elsevier

Brain Research

Volume 655, Issues 1–2, 29 August 1994, Pages 251-254
Brain Research

Short communication
Glucocortcoids mediate the stress-induced extracellular accumulation of glutamate

https://doi.org/10.1016/0006-8993(94)91622-5Get rights and content

Abstract

The hippocampal damage caused by stress has been attributed to an increased glutamatergic tone brought about by secretion of glococorticoids. Although exposure to stress has been shown to increase the outflow of glutamate, direct involvement of glucocorticoid in this phenomenon has not been examined. The present study demonstrates that adrenalectomy attenuates the stress-induced outflow of glutamate in the hippocampus and prefrontal cortex and that glucocorticoid replacement abolishes this attenuation.

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      Glial cells (primarily astrocytes) play a significant role in these alterations as they actively regulate glutamate signaling, by removing glutamate from the synaptic cleft and releasing gliotransmitters acting on NMDA receptors as well as by expressing metabotropic glutamate receptors. Animal studies document that stress exposure induce glutamate release in the hippocampus and PFC (Moghaddam, 1993; Moghaddam et al., 1994; Musazzi et al., 2010) and a consequent downregulation of NMDA receptors (Harvey et al., 2004). At the same time, NMDA receptor activation contributes to the stress-induced inhibition of adult hippocampal neurogenesis (Gould et al., 1997) and to the stress-induced dendritic reorganization of pyramidal cells (Christian et al., 2011; Martin and Wellman, 2011).

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    This work was supported in part by PHS Awards MH48404 (BM), AGO6633 (RMS) and Department of VA National Center for PTSD.

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