Rapid elevations in limbic endocannabinoid content by glucocorticoid hormones in vivo

Matthew N Hill; Ilia N Karatsoreos; Cecilia J Hillard; Bruce S McEwen

doi:10.1016/j.psyneuen.2010.03.005

Back

Rapid elevations in limbic endocannabinoid content by glucocorticoid hormones in vivo

Journal article

Open access

Peer reviewed

Rapid elevations in limbic endocannabinoid content by glucocorticoid hormones in vivo

Matthew N Hill, Ilia N Karatsoreos, Cecilia J Hillard and Bruce S McEwen

Psychoneuroendocrinology, Vol.35(9), pp.1333-1338

2010

DOI: https://doi.org/10.1016/j.psyneuen.2010.03.005

Handle:

https://hdl.handle.net/2376/109062

PMCID: PMC2914801

PMID: 20399021

Files and links (1)

url

https://doi.org/10.1016/j.psyneuen.2010.03.005View

Published (Version of record) Open

Abstract

Non-genomic

FAAH

Cannabinoid

Adrenal

Corticosterone

Limbic

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.

Metrics

15 Record Views

Details

Title: Rapid elevations in limbic endocannabinoid content by glucocorticoid hormones in vivo
Creators: Matthew N Hill - Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
Ilia N Karatsoreos - Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
Cecilia J Hillard - Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
Bruce S McEwen - Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA
Publication Details: Psychoneuroendocrinology, Vol.35(9), pp.1333-1338
Academic Unit: Integrative Physiology and Neuroscience, Department of
Publisher: Elsevier Ltd
Identifiers: 99900547103601842
Language: English
Resource Type: Journal article