Linked Life Data

20939059

Source:http://linkedlifedata.com/resource/pubmed/id/20939059

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-10-12
pubmed:abstractText
Cannabinoid-type 1 (CB1) receptors are implicated in ?-opioid receptor (?-OR)-dependent reward ascribed partially to mesolimbic dopamine release in the nucleus accumbens (Acb) shell. Thus, CB1 receptor gene deletion may preferentially alter the availability of ?-ORs and/or dopamine innervation in this brain region, which is functionally distinct from the motor-associated Acb core. To test this hypothesis, we examined the electron microscopic immunolabeling of the ?-OR and the dopamine-synthesizing enzyme, tyrosine hydroxylase (TH) in Acb shell, and core of adult C57BL/6J wild-type (WT) and CB1-knock-out (KO) mice. The ?-OR-immunogold particles were observed in the cytoplasm and on the plasmalemma in dendrites, dendritic spines, and axon terminals throughout the Acb. Compared to WT, the Acb shell of CB1-KO mice showed a lower cytoplasmic density of ?-ORs in dendrites and fewer ?-OR labeled, but not unlabeled, dendritic spines. In this region, the CB1-KO's had a significantly enhanced plasmalemmal density of ?-OR-immunogold in axon terminals, 70% of which formed excitatory-type synapses. However, the number of both ?-OR-labeled terminals and TH-labeled small varicosities was significantly reduced in the Acb shell of CB1-KO's. These adaptations were not seen in the Acb core, where CB1-KO's had a preferentially lower dendritic plasmalemmal and total spine density of ?-OR immunogold. Our results indicate that constitutive deletion of the CB1 receptor gene has a major impact on the pre and postsynaptic availability of ?-ORs at axospinous synapses and on the dopamine innervation of the Acb shell as well as the dendritic surface expression of ?-ORs in Acb core of mature rodents.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1098-2396
pubmed:author
pubmed:copyrightInfo
© 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
886-97
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Cannabinoid-1 receptor gene deletion has a compartment-specific affect on the dendritic and axonal availability of ?-opioid receptors and on dopamine axons in the mouse nucleus accumbens.
pubmed:affiliation
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural