Linked Life Data

11356924

Source:http://linkedlifedata.com/resource/pubmed/id/11356924

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-5-17
pubmed:abstractText
The role of protein kinase C and intracellular Ca(2+) on amphetamine-mediated dopamine release through the norepinephrine plasmalemmal transporter in undifferentiated PC12 cells was investigated. The selective protein kinase C inhibitor chelerythrine completely inhibited endogenous dopamine release elicited by 1 microM amphetamine. Direct activation of protein kinase C increased dopamine release in a Ca(2+)-insensitive, imipramine-sensitive manner and the release was not additive with amphetamine. Exocytosis was not involved since these events were not altered by either deletion of extracellular Ca(2+) or reserpine pretreatment. Down-regulation of protein kinase C activity by long-term phorbol ester treatment resulted in a dramatic decrease in amphetamine-mediated dopamine release with no apparent effect on [(3)H]dopamine uptake. To more completely examine a role for Ca(2+), intracellular Ca(2+) was chelated in the cells. Depletion of intracellular Ca(2+) considerably decreased dopamine release in response to 1 microM amphetamine compared with vehicle-treated cells, but had no effect on the [(3)H]dopamine uptake. Thus, our results suggest that amphetamine-mediated dopamine release through the plasmalemmal norepinephrine transporter is highly dependent on protein kinase C activity and intracellular but not extracellular Ca(2+). Furthermore, protein kinase C and intracellular Ca(2+) appear to regulate [(3)H]dopamine inward transport and amphetamine-mediated outward transport of dopamine independently in PC12 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1016-24
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11356924-Amphetamine, pubmed-meshheading:11356924-Animals, pubmed-meshheading:11356924-Biological Transport, pubmed-meshheading:11356924-Calcium, pubmed-meshheading:11356924-Carrier Proteins, pubmed-meshheading:11356924-Cell Differentiation, pubmed-meshheading:11356924-Dopamine, pubmed-meshheading:11356924-Down-Regulation, pubmed-meshheading:11356924-Egtazic Acid, pubmed-meshheading:11356924-Enzyme Activation, pubmed-meshheading:11356924-Enzyme Activators, pubmed-meshheading:11356924-Extracellular Space, pubmed-meshheading:11356924-Intracellular Fluid, pubmed-meshheading:11356924-Norepinephrine Plasma Membrane Transport Proteins, pubmed-meshheading:11356924-PC12 Cells, pubmed-meshheading:11356924-Pheochromocytoma, pubmed-meshheading:11356924-Protein Kinase C, pubmed-meshheading:11356924-Rats, pubmed-meshheading:11356924-Symporters, pubmed-meshheading:11356924-Synaptic Vesicles, pubmed-meshheading:11356924-Tetradecanoylphorbol Acetate
pubmed:year
2001
pubmed:articleTitle
Protein kinase C and intracellular calcium are required for amphetamine-mediated dopamine release via the norepinephrine transporter in undifferentiated PC12 cells.
pubmed:affiliation
Department of Pharmacology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.