Linked Life Data

1652179

Source:http://linkedlifedata.com/resource/pubmed/id/1652179

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-9-25
pubmed:abstractText
Calcium uptake reduction in synaptosomes observed in old rats is partly due to a decreased calcium influx through brain voltage-dependent calcium channels. This defect is not due to differences in the polarization of the plasma membrane, but rather to the influx of calcium itself, and may be accentuated at lower concentrations of calcium. We found that the cytosolic calcium concentration in 24-month-old rats is higher than in adults, both at rest and under K-depolarization, and it is suggested that these high calcium levels may partially inactivate synaptosomal calcium channels. The mitochondrial defect may be partially responsible for the increase in cytosolic calcium with age in K-depolarized synaptosomes, but other factors are probably responsible for the increase in resting (Ca2+).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0044-281X
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
88-90
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed:articleTitle
Changes of calcium homeostasis in nerve endings during aging.
pubmed:affiliation
Department of Molecular Biology, CSIC, Autonomous University of Madrid.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't