Linked Life Data

9067454

Source:http://linkedlifedata.com/resource/pubmed/id/9067454

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-5-27
pubmed:abstractText
The distribution of angiotensin II AT1 and AT2 receptor subtypes were mapped in the mouse brain by in vitro autoradiography. Along with a differing distribution of AT1 and AT2 receptors in the hind brain compared to the rat, moderate densities of AT1 receptors were observed in dopamine-rich regions, namely the caudate putamen and nucleus accumbens, previously observed in the human, but not rat or rabbit. Considering our previous anatomical and functional studies demonstrating an interaction between brain angiotensin II and dopaminergic systems, the effect of chronic treatment with the dopamine antagonist, haloperidol, on AT1 and AT2 receptor levels was investigated in the mouse brain. Haloperidol treatment for 21 days resulted in an increase in angiotensin II AT1 receptor levels in the nucleus accumbens, accompanied by an increase in dopamine D2 receptors, but no change in dopamine D1 receptors. Striatal AT1 receptors did not alter with treatment, nor did AT1 or AT2 receptors in a number of brain regions not associated with dopaminergic systems, such as the median preoptic nucleus, paraventricular hypothalamic nucleus, and nucleus of the solitary tract. The present study suggests that brain angiotensin II-dopamine interactions extend beyond the known effects on the nigrostriatal dopaminergic system, to the mesocorticolimbic dopaminergic system.
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
748
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
137-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Upregulation of angiotensin II AT1 receptors in the mouse nucleus accumbens by chronic haloperidol treatment.
pubmed:affiliation
Department of Medicine, University of Melbourne, Victoria, Australia.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't