Linked Life Data

10473264

Source:http://linkedlifedata.com/resource/pubmed/id/10473264

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-10-21
pubmed:abstractText
We examined the effect of ischemia on inositol 1,4,5-trisphosphate receptor-induced Ca2+ release by functional and morphological approaches, using the gerbil model after 6-h unilateral occlusion of the common carotid artery. Autoradiographic study revealed that the basal uptake of 45Ca2+ into the endoplasmic reticulum and caffeine-induced 45Ca2+ release from the endoplasmic reticulum were normal in the presence of ATP in each ischemic brain region, whereas inositol 1,4,5-trisphosphate receptor-induced 45Ca2+ release from the endoplasmic reticulum was inhibited only in the CA1 region of the hippocampus on the ischemic side. In moderately ischemic gerbils, electron microscopic study demonstrated aggregation of swollen endoplasmic reticulum in the CA1 region of the hippocampus, so that abundant endoplasmic reticulum assembled in close contact to form endoplasmic reticulum cisternal stacks. In severely ischemic gerbils, immunohistochemical analysis of the hippocampus showed loss of type 1 inositol 1,4,5-trisphosphate receptor protein with preservation of immunoreactivity for type 2 and 3 inositol 1,4,5-trisphosphate receptor proteins, which was confirmed by western blot analysis. Such selective inhibition of inositol 1,4,5-trisphosphate receptor-induced Ca2+ release and the loss of type 1 inositol 1,4,5-trisphosphate receptor in the CA1 region of the hippocampus in cerebral ischemia may be associated with its region-specific vulnerability to ischemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
93
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
995-1001
pubmed:dateRevised
2007-7-18
pubmed:meshHeading
pubmed-meshheading:10473264-Animals, pubmed-meshheading:10473264-Brain Ischemia, pubmed-meshheading:10473264-Caffeine, pubmed-meshheading:10473264-Calcium Channels, pubmed-meshheading:10473264-Calcium Signaling, pubmed-meshheading:10473264-Carotid Artery, Common, pubmed-meshheading:10473264-Central Nervous System Stimulants, pubmed-meshheading:10473264-Constriction, pubmed-meshheading:10473264-Endoplasmic Reticulum, pubmed-meshheading:10473264-Female, pubmed-meshheading:10473264-Gerbillinae, pubmed-meshheading:10473264-Hippocampus, pubmed-meshheading:10473264-Inositol 1,4,5-Trisphosphate, pubmed-meshheading:10473264-Inositol 1,4,5-Trisphosphate Receptors, pubmed-meshheading:10473264-Male, pubmed-meshheading:10473264-Pyramidal Cells, pubmed-meshheading:10473264-Receptors, Cytoplasmic and Nuclear
pubmed:year
1999
pubmed:articleTitle
Selective inhibition of inositol 1,4,5-triphosphate-induced Ca2+ release in the CA1 region of the hippocampus in the ischemic gerbil.
pubmed:affiliation
Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.
pubmed:publicationType
Journal Article