Linked Life Data

11181943

Source:http://linkedlifedata.com/resource/pubmed/id/11181943

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Our laboratory has developed a technique whereby radiolabeled long-chain fatty acids are injected intravenously in awake rats to pulse-label brain lipids, mainly phospholipids, to measure regional brain lipid metabolism by autoradiography. The brain incorporation of [(3)H]arachidonic acid ([(3)H]AA), a polyunsaturated fatty acid, may reflect regional changes in neurotransmitter signal transduction using phospholipase A(2). Using this radiotracer, we examined the brain dopamine system in rats with a chronic unilateral 6-hydroxydopamine lesion of the substantia nigra pars compacta, a model of Parkinson's disease. Four weeks after lesioning, rats received either vehicle; SKF38393 or quinpirole (LY-171,555) (D(1)- and D(2)-dopamine-like agonists, respectively); or (+)-butaclamol (D(1)/D(2) antagonist) followed by either vehicle, SKF38393, or quinpirole. They then were infused with [(3)H]AA and their brains processed for autoradiography. SKF38393 increased [(3)H]AA incorporation into the lesioned side compared with the intact side in the caudate putamen, somatosensory and motor cortices and subthalamic nucleus, but decreased incorporation in the ipsilateral ventrolateral thalamus. Quinpirole increased ipsilateral [(3)H]AA incorporation in the caudate putamen and somatosensory and motor cortices, and decreased it in the ventrolateral thalamus. (+)-Butaclamol blocked this effect. The data suggest up-regulation in basal ganglia and cortical dopamine circuits mediated by phospholipase A(2) ipsilateral to the substantia nigra lesion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
296
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1074-84
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11181943-2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, pubmed-meshheading:11181943-Animals, pubmed-meshheading:11181943-Arachidonic Acid, pubmed-meshheading:11181943-Biological Markers, pubmed-meshheading:11181943-Disease Models, Animal, pubmed-meshheading:11181943-Dopamine Agonists, pubmed-meshheading:11181943-Male, pubmed-meshheading:11181943-Neurotransmitter Agents, pubmed-meshheading:11181943-Parkinson Disease, pubmed-meshheading:11181943-Phospholipases A, pubmed-meshheading:11181943-Phospholipases A2, pubmed-meshheading:11181943-Rats, pubmed-meshheading:11181943-Rats, Sprague-Dawley, pubmed-meshheading:11181943-Receptors, Dopamine, pubmed-meshheading:11181943-Receptors, Dopamine D1, pubmed-meshheading:11181943-Receptors, Dopamine D2, pubmed-meshheading:11181943-Signal Transduction, pubmed-meshheading:11181943-Tritium
pubmed:year
2001
pubmed:articleTitle
Selective dopamine receptor stimulation differentially affects [3H]arachidonic acid incorporation, a surrogate marker for phospholipase A2-mediated neurotransmitter signal transduction, in a rodent model of Parkinson's disease.
pubmed:affiliation
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA.
pubmed:publicationType
Journal Article