Linked Life Data

9427516

Source:http://linkedlifedata.com/resource/pubmed/id/9427516

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1998-2-17
pubmed:abstractText
The association between the beta1 subunit and the alpha subunit of the sodium channel from rat brain was studied in hippocampus during postnatal development and in cultures of fetal rat forebrain neurons and cerebellar granule cells, using an anti-beta1 antipeptide antibody to specifically immunoprecipitate alphabeta1 complexes labeled with [3H]saxitoxin. In the hippocampus, the increase in beta1 RNA expression during development was accompanied by an increase in immunoprecipitated alphabeta1 complexes. Most of the alphabeta1 complexes were constituted during the first 3 postnatal weeks, with the steepest rise between postnatal days 5 and 12. In cultured fetal neurons, the amount of beta1 RNA and of alphabeta1 complexes was approximately 3-4% of that found in the adult, whereas it reached 60-70% in cultured cerebellar granule cells. We had previously described a neurotoxin-induced internalization of sodium channels which occurred in immature neurons but not in adult tissue. Internalization decreased during development in neurotoxin-treated hippocampal slices, and resistance of plasma membrane sodium channels to internalization followed the same time course than the appearance of alphabeta1 complexes. Similarly, neurotoxin activation resulted in sodium channel internalization in fetal neurons, while cerebellar granule cells, which express high levels of beta1 RNA and of alphabeta1 complexes, did not internalize their [3H]saxitoxin receptors in that same conditions. These data suggested that the association of the beta1 subunit with the alpha subunit could provide a suitable marker for the stabilization and anchoring of sodium channels in discrete membrane domains which occur during neuronal development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0169-328X
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-53
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Down-regulation of voltage-dependent sodium channels coincides with a low expression of alphabeta1 subunit complexes.
pubmed:affiliation
INSERM U464, Institut Jean Roche, Faculté de Médecine Secteur Nord, Marseille, France. alcaraz.g@jean-roche.univ.mrs.fr
pubmed:publicationType
Journal Article