Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-6-29
pubmed:abstractText
A homozygous CGRP-/- mouse line was generated by the targeted disruption of exon 5 in the calcitonin/alphaCGRP gene using homologous recombination. The mutant mice lack alphaCGRP mRNA. Furthermore CGRP immunoreactivity almost completely disappears from the spinal cord and is not at all observed in spinal ganglia and muscle synapses. However, motor end plates were still detected by acetylcholinesterase staining. Antinociceptive behavior tested by the tail flick and hot plate tests did not significantly differ in mutant and wild-type mice, except when challenged by morphine. Paradoxically, morphine analgesia was reduced in mutant mice compared with controls in the tail flick test, but not in the hot plate test. Thus, alphaCGRP differentially modulates opiate pain pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
849-54
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Modulation of morphine analgesia in alphaCGRP mutant mice.
pubmed:affiliation
CNRS UA D1284 Neurobiologie Moléculaire, Institut Pasteur, Paris, France.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't