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Prolonged glucocorticoid treatment decreases cannabinoid CB 1 receptor density in the hippocampus
Author(s) -
Hill Matthew N.,
Carrier Erica J.,
Ho W.S. Vanessa,
Shi Leyu,
Patel Sachin,
Gorzalka Boris B.,
Hillard Cecilia J.
Publication year - 2008
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20386
Subject(s) - endocannabinoid system , cannabinoid , cannabinoid receptor , corticosterone , hippocampal formation , glucocorticoid , anandamide , medicine , endocrinology , hippocampus , agonist , chemistry , glucocorticoid receptor , depolarization induced suppression of inhibition , receptor , pharmacology , hormone
Experimental studies indicate a bidirectional, functional relationship between glucocorticoids and the endocannabinoid system; however, the effects of repeated glucocorticoid treatment on the endocannabinoid system have not been examined. In this study, we treated male rats with either a single dose or a 21‐day course of treatment with corticosterone (20 mg/kg) and measured hippocampal cannabinoid CB 1 receptor expression and endocannabinoid content. The 21‐day, but not the single, administration of corticosterone significantly reduced both the binding site density and amount of protein of the hippocampal cannabinoid CB 1 receptor without affecting affinity for the CB 1 receptor agonist, [ 3 H]CP55940. With regard to hippocampal endocannabinoid content, acute corticosterone treatment resulted in a significant reduction in anandamide but did not affect 2‐arachidonylglycerol, while repeated corticosterone treatment did not alter content of either anandamide or 2‐arachidonylglycerol. These data support the hypothesis that the cannabinoid CB 1 receptor is under negative regulation by glucocorticoids in the hippocampus, and suggest that hippocampal cannabinoid CB 1 receptor signaling could be reduced under conditions associated with hypersecretion of glucocorticoids, such as chronic stress. © 2007 Wiley‐Liss, Inc.