Linked Life Data

10493768

Source:http://linkedlifedata.com/resource/pubmed/id/10493768

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
1999-10-14
pubmed:abstractText
The membrane density of L-type voltage-sensitive Ca(2+) channels (L-VSCCs) of rat hippocampal neurons increases over age [days in vitro (DIV)] in long-term primary cultures, apparently contributing both to spontaneous cell death and to enhanced excitotoxic vulnerability. Similar increases in L-VSCCs occur during brain aging in vivo in rat and rabbit hippocampal neurons. However, unraveling both the molecular basis and the functional implications of these age changes in VSCC density will require determining whether the other types of high-threshold VSCCs (e.g., N, P/Q, and R) also exhibit altered density and/or changes in regulation, for example, by the important G-protein-coupled, membrane-delimited inhibitory pathway. These possibilities were tested here in long-term hippocampal cultures. Pharmacologically defined whole-cell currents were corrected for cell size differences over age by normalization with whole-cell capacitance. The Ca(2+) channel current density (picoamperes per picofarad), mediated by each Ca(2+) channel type studied here (L, N, and a combined P/Q + R component), increased through 7 DIV. Thereafter, however, only L-type current density continued to increase, at least through 21 DIV. Concurrently, pertussis toxin-sensitive G-protein-coupled inhibition of non-L-type Ca(2+) channel current induced by the GABA(B) receptor agonist baclofen or by guanosine 5'-3-O-(thio)triphosphate declined dramatically with age in culture. Thus, the present studies identify selective and novel parallel mechanisms for the time-dependent alteration of Ca(2+) influx, which could importantly influence function and vulnerability during development and/or aging.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8674-84
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10493768-Animals, pubmed-meshheading:10493768-Baclofen, pubmed-meshheading:10493768-Calcium Channels, pubmed-meshheading:10493768-Calcium Channels, L-Type, pubmed-meshheading:10493768-Cell Aging, pubmed-meshheading:10493768-Cell Division, pubmed-meshheading:10493768-Cells, Cultured, pubmed-meshheading:10493768-Fetus, pubmed-meshheading:10493768-GABA-B Receptor Agonists, pubmed-meshheading:10493768-GTP-Binding Proteins, pubmed-meshheading:10493768-Guanosine 5'-O-(3-Thiotriphosphate), pubmed-meshheading:10493768-Hippocampus, pubmed-meshheading:10493768-Neurons, pubmed-meshheading:10493768-Nimodipine, pubmed-meshheading:10493768-Patch-Clamp Techniques, pubmed-meshheading:10493768-Peptides, pubmed-meshheading:10493768-Rabbits, pubmed-meshheading:10493768-Rats, pubmed-meshheading:10493768-Rats, Sprague-Dawley, pubmed-meshheading:10493768-Tetrodotoxin, pubmed-meshheading:10493768-omega-Conotoxin GVIA
pubmed:year
1999
pubmed:articleTitle
Decreased G-protein-mediated regulation and shift in calcium channel types with age in hippocampal cultures.
pubmed:affiliation
Department of Pharmacology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.