RRC ID 21269
著者 Tian X, Zhou Y, Gao L, He G, Jiang W, Li W, Takahashi E.
タイトル Analysis of ischemic neuronal injury in Cav2.1 channel α1 subunit mutant mice.
ジャーナル Biochem Biophys Res Commun
Abstract One of the main instigators leading to cell death and brain damage following ischemia is Ca(2+) dysregulation. Neuronal membrane depolarization results in the activation of voltage-gated Ca(2+) (CaV) channels and intracellular Ca(2+) influx. We investigated the physiological role of the CaV2.1 (P/Q-type) channel in ischemic neuronal injury using CaV2.1 channel α1 subunit mutant mice, rolling Nagoya and leaner mice. The in vivo ischemia model with a complete occlusion of the middle cerebral artery showed that the infarct area at 24h was significantly smaller in rolling Nagoya (27.1±3.5% of total brain volume) and leaner (20.1±3.5%) mice compared to wild-type (42.9±4.5%) mice. In an in vitro Ca(2+) imaging study, oxygen-glucose deprivation using a hippocampal slice induced a significantly slower rate of increase in intracellular Ca(2+) concentration ([Ca(2+)]i) in rolling Nagoya (0.083±0.007/min) and leaner (0.062±0.006/min) mice compared to wild-type (0.105±0.008/min) mice. These results demonstrate that the mutant CaV2.1 channel in rolling Nagoya and leaner mice plays a different protective role in a ([Ca(2+)]i)-dependent manner in ischemic models and indicate that CaV2.1 channel blockers may be used preventively against ischemic injury.
巻・号 434(1)
ページ 60-4
公開日 2013-4-26
DOI 10.1016/j.bbrc.2013.03.066
PII S0006-291X(13)00520-2
PMID 23545255
MeSH Animals Brain Ischemia / genetics Brain Ischemia / pathology* Brain Ischemia / physiopathology* Calcium Channel Blockers / pharmacology Calcium Channels, N-Type / genetics* Calcium Channels, N-Type / physiology Disease Models, Animal Male Mice Mice, Inbred C57BL Mice, Mutant Strains Neurons / drug effects Neurons / pathology Protein Subunits / genetics Protein Subunits / physiology
IF 2.985
引用数 9
WOS 分野 BIOPHYSICS BIOCHEMISTRY & MOLECULAR BIOLOGY
リソース情報
実験動物マウス RBRC00388