Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2007-4-18
pubmed:abstractText
1. Recent studies have suggested that the basolateral nucleus of the amygdala (BLA) participates in the processing of pain information, especially noxious somatic information. Cannabinoid receptors or CB1 mRNA are expressed more in the BLA than in other nuclei of the amygdala. Thus, the aim of the present study was to examine whether CB1 receptors in the BLA may be involved in modulating acute and/or tonic nociceptive processing. 2. Adult rats were exposed to intra-BLA microinjection of the cannabinoid receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl) pyrrolo [1,2,3,-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate [WIN 55,212-2 (1, 2.5, 5 or 10 microg/side)] and subjected to the tail flick and formalin tests. 3. The rats demonstrated a dose-dependent increase in latency to withdraw from a thermal noxious stimulus in the tail flick test and a decrease in formalin-induced pain behaviours. The antinociceptive effects of the CB1 receptor agonist WIN 55,212-2 (10 microg/side) in both tests were attenuated in the presence of the selective CB1 receptor antagonist, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3- carboxamide (AM251; 0.55 ng/side). Administration of the CB1 receptor antagonist AM251 (0.55, 5.5, or 55.5 ng/side) alone did not alter the nociceptive thresholds in either test. Bilateral microinjection of the selective CB2 receptor antagonist N-[(1S)-endo-1,3,3-trimethyl bicyclo [2.2.1] heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; 1 microg/side) had no effect on the antinociception produced by WIN 55,212-2, suggesting that the antinociceptive actions of WIN 55,212-2 are mediated by CB1 receptors. 4. The findings suggest the existence of a CB1-mediated inhibitory system in the BLA that, when activated, can diminish responsivity to acute and tonic noxious stimuli, but that normally has no tonic effect on the response threshold of these stimuli.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0305-1870
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
439-49
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17439413-Amygdala, pubmed-meshheading:17439413-Analgesics, pubmed-meshheading:17439413-Animals, pubmed-meshheading:17439413-Benzoxazines, pubmed-meshheading:17439413-Bornanes, pubmed-meshheading:17439413-Dose-Response Relationship, Drug, pubmed-meshheading:17439413-Hot Temperature, pubmed-meshheading:17439413-Male, pubmed-meshheading:17439413-Microinjections, pubmed-meshheading:17439413-Models, Anatomic, pubmed-meshheading:17439413-Morpholines, pubmed-meshheading:17439413-Motor Activity, pubmed-meshheading:17439413-Naphthalenes, pubmed-meshheading:17439413-Pain, pubmed-meshheading:17439413-Pain Measurement, pubmed-meshheading:17439413-Piperidines, pubmed-meshheading:17439413-Pyrazoles, pubmed-meshheading:17439413-Rats, pubmed-meshheading:17439413-Rats, Wistar, pubmed-meshheading:17439413-Receptor, Cannabinoid, CB1, pubmed-meshheading:17439413-Receptor, Cannabinoid, CB2, pubmed-meshheading:17439413-Tail
pubmed:articleTitle
CB1 receptor activation in the basolateral amygdala produces antinociception in animal models of acute and tonic nociception.
pubmed:affiliation
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran.
pubmed:publicationType
Journal Article