| pubmed-article:14742725 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0086376 | lld:lifeskim |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:14742725 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:14742725 | pubmed:issue | Pt 1 | lld:pubmed |
| pubmed-article:14742725 | pubmed:dateCreated | 2004-4-6 | lld:pubmed |
| pubmed-article:14742725 | pubmed:abstractText | N-type voltage-dependent Ca(2+) channels (N-VDCCs) play important roles in neurotransmitter release and certain postsynaptic phenomena. These channels are modulated by a number of intracellular factors, notably by Gbetagamma subunits of G proteins, which inhibit N-VDCCs in a voltage-dependent (VD) manner. Here we show that an increase in intracellular Na(+) concentration inhibits N-VDCCs in hippocampal pyramidal neurones and in Xenopus oocytes. In acutely dissociated hippocampal neurones, Ba(2+) current via N-VDCCs was inhibited by Na(+) influx caused by the activation of NMDA receptor channels. In Xenopus oocytes expressing N-VDCCs, Ba(2+) currents were inhibited by Na(+) influx and enhanced by depletion of Na(+), after incubation in a Na(+)-free extracellular solution. The Na(+)-induced inhibition was accompanied by the development of VD facilitation, a hallmark of a Gbetagamma-dependent process. Na(+)-induced regulation of N-VDCCs is Gbetagamma dependent, as suggested by the blocking of Na(+) effects by Gbetagamma scavengers and by excess Gbetagamma, and may be mediated by the Na(+)-induced dissociation of Galphabetagamma heterotrimers. N-VDCCs may be novel effectors of Na(+)ion, regulated by the Na(+) concentration via Gbetagamma. | lld:pubmed |
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| pubmed-article:14742725 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14742725 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14742725 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14742725 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14742725 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14742725 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:14742725 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:DascalNathanN | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:BlumensteinYa... | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:KanevskyNatal... | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:KrishtalOlegO | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:MaximyukOlexa... | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:LozovayaNatal... | lld:pubmed |
| pubmed-article:14742725 | pubmed:author | pubmed-author:YatsenkoNatal... | lld:pubmed |
| pubmed-article:14742725 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14742725 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:14742725 | pubmed:volume | 556 | lld:pubmed |
| pubmed-article:14742725 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14742725 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14742725 | pubmed:pagination | 121-34 | lld:pubmed |
| pubmed-article:14742725 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
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| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:meshHeading | pubmed-meshheading:14742725... | lld:pubmed |
| pubmed-article:14742725 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14742725 | pubmed:articleTitle | Intracellular Na+ inhibits voltage-dependent N-type Ca2+ channels by a G protein betagamma subunit-dependent mechanism. | lld:pubmed |
| pubmed-article:14742725 | pubmed:affiliation | Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel. dascaln@post.tau.ac.il | lld:pubmed |
| pubmed-article:14742725 | pubmed:publicationType | Journal Article | lld:pubmed |
