Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-1-31
pubmed:abstractText
Mesocorticolimbic dopaminergic systems subserve cognitive processes, motivated behavior, the central stress response, and the reinforcing properties of drugs of abuse. Hyperdopaminergic states have been suggested to contribute to the psychotropic effects of the cannabinoids; however, the mechanisms by which cannabinoids activate mesocorticolimbic dopaminergic systems are not well understood. We have examined the role of noradrenergic neurotransmission in the mediation of cannabinoid-induced activation of A10 dopaminergic neurons using Fos as a marker of neuronal activation in mice. Administration of the CB(1) receptor agonist CP55940 differentially increased the number of Fos-like immunoreactive (Fos-li) A10 dopaminergic cells within three anatomically distinct regions (parabrachial pigmented, paranigral, and caudal linear nuclei) compared to vehicle-treated mice. Similar results were obtained using the CB(1) receptor agonist Win 55212-2; and pretreatment with the CB(1) receptor antagonist SR141716 significantly inhibited CP55940-induced Fos expression. Pretreatment with the alpha(1)-adrenergic receptor antagonist, prazosin, and the alpha(2)-adrenergic receptor agonist, clonidine, reduced the number of Fos-li dopaminergic neurons induced by CP55940 in a subregion-specific manner. CP55940 and Win 55212-2 increased the number of Fos-li neurons within the locus coeruleus. Finally, CB(1) receptor immunoreactivity was detected on fibers within the CL but not in either PBP or PN. Our data demonstrate that cannabinoids induce Fos expression within A10 dopaminergic neurons in a heterogeneous anatomical pattern, and suggest that enhanced noradrenergic neurotransmission contributes to cannabinoid-induced activation of A10 dopaminergic neurons in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
963
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15-25
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12560108-Adrenergic alpha-Agonists, pubmed-meshheading:12560108-Adrenergic alpha-Antagonists, pubmed-meshheading:12560108-Animals, pubmed-meshheading:12560108-Cannabinoids, pubmed-meshheading:12560108-Cerebral Cortex, pubmed-meshheading:12560108-Clonidine, pubmed-meshheading:12560108-Cyclohexanols, pubmed-meshheading:12560108-Dopamine, pubmed-meshheading:12560108-Gene Expression Regulation, pubmed-meshheading:12560108-Genes, fos, pubmed-meshheading:12560108-Immunohistochemistry, pubmed-meshheading:12560108-Limbic System, pubmed-meshheading:12560108-Locus Coeruleus, pubmed-meshheading:12560108-Male, pubmed-meshheading:12560108-Mice, pubmed-meshheading:12560108-Mice, Inbred ICR, pubmed-meshheading:12560108-Neurons, pubmed-meshheading:12560108-Norepinephrine, pubmed-meshheading:12560108-Prazosin, pubmed-meshheading:12560108-Receptors, Cannabinoid, pubmed-meshheading:12560108-Receptors, Drug, pubmed-meshheading:12560108-Synaptic Transmission
pubmed:year
2003
pubmed:articleTitle
Cannabinoid-induced Fos expression within A10 dopaminergic neurons.
pubmed:affiliation
Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.