Journal
BRAIN RESEARCH
Volume 1339, Issue -, Pages 18-25Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2010.03.105
Keywords
Neuropathic pain; Cannabinoid; Rostral anterior cingulate cortex; WIN 55,212-2
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Funding
- NIH [T32DA07027, R01DA020836, R01DA014277, K05DA000480]
- Institute of International Education, Scholar Rescue Funds, New York
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The present studies examined the effect of chronic neuropathic pain on cannabinoid receptor density and receptor-mediated G-protein activity within supraspinal brain areas involved in pain processing and modulation in mice. Chronic constriction injury (CCI) produced a significant decrease in WIN 55,212-2-stimulated [S-35]GTP gamma S binding in membranes prepared from the rostral anterior cingulate cortex (rACC) of CCI mice when compared to sham-operated controls. Saturation binding with [H-3]SR 141716A in membranes of the rACC showed no significant differences in binding between CCI and sham mice. Analysis of levels of the endocannabinoids anandamide (AEA) or 2-arachidonoylglycerol (2-AG) in the rACC following CCI showed no significant differences between CCI and sham mice. These data suggest that CCI produced desensitization of the cannabinoid 1 receptor in the rACC in the absence of an overall decrease in cannabinoid 1 receptor density or change in levels of AEA or 2-AG. These data are the first to show alterations in cannabinoid receptor function in the rostral anterior cingulate cortex in response to a model of neuropathic pain. (C) 2010 Elsevier B.V. All rights reserved.
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