Rapid elevations in limbic endocannabinoid content by glucocorticoid hormones in vivo

PSYCHONEUROENDOCRINOLOGY

卷:35

Article

Hill, Matthew N.¹  Karatsoreos, Ilia N.¹  Hillard, Cecilia J.²  McEwen, Bruce S.¹ 

[1] Rockefeller Univ, Neuroendocrinol Lab, New York, NY 10065 USA

[2] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA

关键词: FAAH;    Non-genomic;    Limbic;    Cannabinoid;    Corticosterone;    Adrenal;   

DOI  :  10.1016/j.psyneuen.2010.03.005

来源: Elsevier

【 摘 要 】

Functional interactions between glucocorticoids and the endocannabinoid system have been repeatedly documented; yet, to date, no studies have demonstrated in vivo that glucocorticoid hormones regulate endocannabinoid signaling. We demonstrate that systemic administration of the glucocorticoid corticosterone (3 and 10 mg/kg) resulted in an increase in the tissue content of the endocannabinoid N-arachidonylethanolamine (AEA) within several limbic structures (amygdala, hippocampus, hypothalamus), but not the prefrontal cortex, of male rats. Tissue AEA content was increased at 10 min and returned to control 1 h post-corticosterone administration. The other primary endocannabinoid, 2-arachidonoylglycerol, was found to be elevated by corticosterone exclusively within the hypothalamus. The rapidity of the change suggests that glucocorticoids act through a non-genomic pathway. Tissue contents of two other N-acylethanolamines, palmitoylethanolamide and oleolyethanolamide, were not affected by corticosterone treatment, suggesting that the mechanism of regulation is neither fatty acid amide nor N-acylphosphatidylethanolamine phospholipase D. These data provide in vivo support for non-genomic steroid effects in mammals and suggest that AEA is a mediator of these effects. (C) 2010 Elsevier Ltd. All rights reserved.

【 授权许可】

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