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Titolo:
DOPAMINERGIC MODULATION OF SODIUM CURRENT IN HIPPOCAMPAL-NEURONS VIA CAMP-DEPENDENT PHOSPHORYLATION OF SPECIFIC SITES IN THE SODIUM-CHANNELALPHA-SUBUNIT
Autore:
CANTRELL AR; SMITH RD; GOLDIN AL; SCHEUER T; CATTERALL WA;
Indirizzi:
UNIV WASHINGTON,DEPT PHARMACOL,BOX 357280 SEATTLE WA 98195 UNIV WASHINGTON,DEPT PHARMACOL SEATTLE WA 98195 UNIV CALIF IRVINE,DEPT MICROBIOL & MOL GENET IRVINE CA 92697
Titolo Testata:
The Journal of neuroscience
fascicolo: 19, volume: 17, anno: 1997,
pagine: 7330 - 7338
SICI:
0270-6474(1997)17:19<7330:DMOSCI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; RAT STRIATAL NEURONS; CA1 PYRAMIDAL CELLS; SELECTIVE PHOSPHORYLATION; TRANSFECTED CELLS; XENOPUS OOCYTES; RECEPTORS; IDENTIFICATION; AGONISTS; INVITRO;
Keywords:
NA+ CURRENT; NEUROMODULATION; CAMP-DEPENDENT PROTEIN KINASE; HIPPOCAMPUS; DOPAMINE RECEPTORS; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
A.R. Cantrell et al., "DOPAMINERGIC MODULATION OF SODIUM CURRENT IN HIPPOCAMPAL-NEURONS VIA CAMP-DEPENDENT PHOSPHORYLATION OF SPECIFIC SITES IN THE SODIUM-CHANNELALPHA-SUBUNIT", The Journal of neuroscience, 17(19), 1997, pp. 7330-7338

Abstract

Phosphorylation of brain Na+ channel alpha subunits by cAMP-dependentprotein kinase (PKA) decreases peak Na+ current in cultured brain neurons and in mammalian cells and Xenopus oocytes expressing cloned brain Na+ channels. We have studied PKA regulation of Na+ channel functionby activation of D1-like dopamine receptors in acutely isolated hippocampal neurons using whole-cell voltage-clamp recording techniques. The D1 agonist SKF 81297 reversibly reduced peak Na+ current in a concentration-dependent manner. No changes in the voltage dependence or kinetics of activation or inactivation were observed. This effect was mediated by PKA, as it was mimicked by application of the PKA activator ofuranosylbenzimidazole-3',5'-monophosphorothioate (cBIMPS) and was inhibited by the specific PKA inhibitor peptide PKAI(5-24). cBIMPS had similar effects on type IIA brain Na+ channel alpha subunits expressed intsA-201 cells, but no effect was observed on a mutant Na+ channel alpha subunit in which serine residues in five PKA phosphorylation sites in the intracellular loop connecting domains I and II (LI-II) had beenreplaced by alanine, A single mutation, S573A, similarly eliminated cBIMPS modulation, Thus, activation of D1-like dopamine receptors results in PKA-dependent phosphorylation of specific sites in LI-II of the Na+ channel alpha subunit, causing a reduction in Na+ current. Such modulation is expected to exert a profound influence on overall neuronalexcitability. Dopaminergic input to the hippocampus from the mesocorticolimbic system may exert this influence in vivo.

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Documento generato il 20/09/20 alle ore 19:09:54