Sustained glucocorticoid exposure recruits cortico-limbic CRH signaling to modulate endocannabinoid function
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- 作者：J. Megan Graya ; b ; c ; e ; Christopher D. Wilsonf ; Tiffany T.Y. Leea ; g ; Quentin J. Pittmana ; b ; e ; Jan M. Deussingh ; Cecilia J. Hillardi ; Bruce S. McEwenf ; Jay Schulkinj ; Ilia N. Karatsoreosk ; Sachin Patell ; Matthew N. Hilla ; b ; c ; d ; mnhill@ucalgary.ca" class="auth_mail" title="E-mail the corresponding author
- 关键词：ACTH ; adrenocorticotropic hormone ; AEA ; N-arachidonylethanolamine ; CB1 ; cannabinoid type 1 receptor ; CORT ; corticosterone ; CRH ; corticotropin-releasing hormone ; CRHR1 ; CRH receptor type 1 ; CRH-OE ; CRH overexpressing mice ; FAAH ; fatty acid amide hydrolase ; GABA ; gamma-aminobutyric acid ; PFC ; prefrontal cortex ; WT ; wild-type ; 2-AG ; 2-arachidonoylglycerol
- 刊名：Psychoneuroendocrinology
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：66
- 期：Complete
- 页码：151-158
- 全文大小：1048 K
文摘
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Chronic elevations in corticosterone (CORT) modulate endocannabinoid levels.
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CORT-induced changes in endocannabinoids are mediated by CRH signaling.
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Chronic overexpression of CRH modulates endocannabinoids similar to chronic CORT.