Linked Life Data

12686757

Source:http://linkedlifedata.com/resource/pubmed/id/12686757

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-4-10
pubmed:abstractText
Noda epileptic rat (NER) is a mutant rat, which spontaneously exhibits a tonic-clonic convulsion from 14 weeks of age. An intracellular recording study was performed to elucidate the abnormal excitability of NER hippocampal CA3 neurons. The recorded neurons were classified into two groups, group A and B neurons, according to the responses to a single stimulation of mossy fibers. In group A neurons, a stimulus elicited a long-lasting depolarization shift accompanying repetitive firings followed by after-hyperpolarization. In group B neurons, the same stimulus elicited a single spike without a long-lasting depolarization shift. Bath application of 1 mM Cd(2+), a nonselective Ca(2+) channel blocker, completely inhibited the abnormal excitation in group A neurons. We further examined the character of Ca(2+) spikes in NER CA3 neurons. Ca(2+) spikes were completely blocked by 10 microM Cd(2+) in group A neurons, but not in either group B or control neurons, suggesting that Ca(2+) channels in NER group A neurons have the hypersensitivity to Cd(2+). Analysis using subtype specific blockers of Ca(2+) channel raised the possible involvement of T-type Ca(2+) channels. These results suggest that Ca(2+) channel dysfunction is involved in the abnormal excitability of CA3 pyramidal neurons and pathogenesis of epilepsy in NER.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1347-8613
pubmed:author
pubmed:issnType
Print
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
137-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Involvement of Ca(2+) channels in abnormal excitability of hippocampal CA3 pyramidal cells in noda epileptic rats.
pubmed:affiliation
Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
pubmed:publicationType
Journal Article, In Vitro