Journal
NEUROSCIENCE LETTERS
Volume 397, Issue 3, Pages 180-184Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2005.12.008
Keywords
2-AG; anandamide; antinociception; FAAH; MGL; periaqueductal gray
Categories
Funding
- NIDA NIH HHS [DA14265, DA3412, DA12447, DA14022] Funding Source: Medline
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Recent work in our laboratories has demonstrated that an opioid-independent form of stress-induced analgesia (SIA) is mediated by endogenous ligands for cannabinoid receptors-anandamide and 2-arachidonoylglycerol (2-AG) [A.G. Hohmann, R.L. Suplita, N.M. Bolton, M.H. Neely, D. Fegley, R. Mangieri, J.F. Krey, J.M. Walker, P.V. Holmes, J.D. Crystal, A. Durand, A. Tontini, M. Mor, G. Tarzia, D. Piomelli, An endocannabinoid mechanism for stress-induced analgesia, Nature 435 (2005) 1108-1112]. The present study was conducted to examine the contribution of cannabinoid CB I receptors in the basolateral nucleus of the amygdala (BLA) and central nucleus of the amygdala (CeA) to nonopioid SIA. SIA was induced by continuous footshock (3 min 0.9 mA) and quantified behaviorally using the tail-flick test. Microinjection of the CB, antagonist/inverse agonist rimonabant (SR141716A) into the BLA, a limbic forebrain region with high densities of CB, receptors, suppressed SIA relative to control conditions. By contrast, the same dose administered into the CeA, where CB 1 immunoreactivity is largely absent, or outside the amygdala did not alter SIA. To examine the contribution of endocannabinoids in the BLA to SIA, we used selective pharmacological inhibitors of the anandamide-degrading enzyme fatty-acid amide hydrolase (FAAH) and the 2-arachidonoylglycerol-degrading enzyme monoacylglycerol lipase (MGL). The FAAH inhibitor URB597 and MGL inhibitor URB602, at doses that enhanced SIA following microinjection in the midbrain periaqueductal gray, did not alter SIA relative to control conditions. Our findings suggest that CB, receptors in the BLA but not the CeA contribute to SIA, but pharmacological inhibition of endocannabinoid degradation at these sites does not affect the expression of stress antinociception. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
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