| First Author | Tian X | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 434 |
| Issue | 1 | Pages | 60-4 |
| PubMed ID | 23545255 | Mgi Jnum | J:201208 |
| Mgi Id | MGI:5512793 | Doi | 10.1016/j.bbrc.2013.03.066 |
| Citation | Tian X, et al. (2013) Analysis of ischemic neuronal injury in Cav2.1 channel alpha1 subunit mutant mice. Biochem Biophys Res Commun 434(1):60-4 |
| abstractText | 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 alpha1 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. |
