| pubmed-article:16935424 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C0242402 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C0521329 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C0006669 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C1172779 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C0278080 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:16935424 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:16935424 | pubmed:issue | 1-3 | lld:pubmed |
| pubmed-article:16935424 | pubmed:dateCreated | 2006-11-22 | lld:pubmed |
| pubmed-article:16935424 | pubmed:abstractText | Studies implicate endocannabinoids in the acute and chronic actions of opioid drugs, including the genesis of physical dependence. Previous evidence suggests that spinal release of calcitonin gene-related peptide (CGRP) and activation of its receptors contribute to opioid physical dependence. The release of CGRP at the spinal level is modulated by cannabinoid (CB1)-receptors. Thus, this study examined whether CB1-receptor activity mediates changes in CGRP underlying development of opioid physical dependence. Systemic morphine administration for 5-days elevated CGRP-immunoreactivity in the rat spinal dorsal horn. In situ hybridization of dorsal root ganglion (DRG) neurons revealed an increase in CGRP mRNA during initial (day 1-3) but not later phase (day 4-5) of morphine treatment. CGRP-immunoreactivity in DRG neurons, however, was increased in the later phase of morphine treatment. Naloxone challenge to morphine-treated animals precipitated an intense withdrawal syndrome that depleted CGRP-immunoreactivity and increased Fos expression in the dorsal horn. The Fos-response primarily occurred in neurons that expressed CGRP receptor component protein (RCP) suggesting CGRP activity contributes to neuronal activation during precipitated withdrawal. Spinal slices obtained from morphine-treated animals showed higher levels of CGRP release than from saline controls. Intrathecal co-administration of CB1-receptor antagonists, AM-251 or SR141716A, with daily morphine attenuated the behavioral manifestations of withdrawal. Treatment with AM-251 also reduced the depletion of CGRP, suppressed Fos-induction, and prevented the increase in capsaicin-evoked spinal CGRP release. Altogether, this study suggests that endocannabinoid activity, expressed via CB1-receptors, contributes to the induction of opioid physical dependence through spinal modulation of CGRP. | lld:pubmed |
| pubmed-article:16935424 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16935424 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16935424 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16935424 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:16935424 | pubmed:issn | 1872-6623 | lld:pubmed |
| pubmed-article:16935424 | pubmed:author | pubmed-author:ChabotJean-Gu... | lld:pubmed |
| pubmed-article:16935424 | pubmed:author | pubmed-author:JhamandasKhem... | lld:pubmed |
| pubmed-article:16935424 | pubmed:author | pubmed-author:MaWeiyaW | lld:pubmed |
| pubmed-article:16935424 | pubmed:author | pubmed-author:TrangTuanT | lld:pubmed |
| pubmed-article:16935424 | pubmed:author | pubmed-author:QuirionRemiR | lld:pubmed |
| pubmed-article:16935424 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:16935424 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16935424 | pubmed:volume | 126 | lld:pubmed |
| pubmed-article:16935424 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16935424 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16935424 | pubmed:pagination | 256-71 | lld:pubmed |
| pubmed-article:16935424 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16935424 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16935424 | pubmed:articleTitle | Spinal modulation of calcitonin gene-related peptide by endocannabinoids in the development of opioid physical dependence. | lld:pubmed |
| pubmed-article:16935424 | pubmed:affiliation | Department of Pharmacology and Toxicology and Anesthesiology, Queen's University Kingston, Ont., Canada K7L 3N6. | lld:pubmed |
| pubmed-article:16935424 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16935424 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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