Gentile N T, Spatz M, Brenner M, McCarron R M, Hallenbeck J M
Stroke Branch, NINDS, National Institutes of Health, Bethesda, Maryland 20892-4128, USA.
Neurochem Res. 1996 Aug;21(8):947-54. doi: 10.1007/BF02532345.
Resting and depolarization-induced 45CaCl2 accumulation was compared for synaptosomes isolated from hibernating and nonhibernating ground squirrels. Channel subtype antagonists were used to identify the active voltage-sensitive calcium channel subtypes in these preparations. There was significantly less 45Ca2+ accumulation in synaptosomes isolated from hibernating as compared to cold-adapted nonhibernating ground squirrels in both basal (p < 0.005) and depolarizing (p < 0.03) media over a 30 sec to 5 min incubation period. The elevation in 45Ca2+ accumulation triggered by K+ depolarization was blocked by 50 microM CdCl2, 1 microM omega-conotoxin MVIIC or 1 microM omega-agatoxin IVA. Inhibition was not observed with 1 microM nifedipine or with 1 microM omega-conotoxin GVIA. These results suggest that hibernation is associated with reduced presynaptic 45Ca2+ conductance via voltage-sensitive channels with a pharmacological sensitivity that is different from the established L-, N-, and P-types in other systems but share features of the recently described Q-type calcium channel. This decrease may reflect a cellular adaptation that helps confer tolerance to the near total cerebral ischemia associated with hibernation.
比较了从冬眠和非冬眠地松鼠分离出的突触体的静息和去极化诱导的45CaCl2积累。使用通道亚型拮抗剂来鉴定这些制剂中活性电压敏感钙通道的亚型。在30秒至5分钟的孵育期内，与冷适应的非冬眠地松鼠分离出的突触体相比，从冬眠地松鼠分离出的突触体在基础培养基（p < 0.005）和去极化培养基（p < 0.03）中45Ca2+的积累明显较少。50 microM CdCl2、1 microM ω-芋螺毒素MVIIC或1 microM ω-阿加毒素IVA可阻断由K+去极化触发的45Ca2+积累升高。1 microM硝苯地平或1 microM ω-芋螺毒素GVIA未观察到抑制作用。这些结果表明，冬眠与通过电压敏感通道的突触前45Ca2+电导降低有关，其药理学敏感性不同于其他系统中已确定的L型、N型和P型，但具有最近描述的Q型钙通道的特征。这种减少可能反映了一种细胞适应性，有助于赋予对与冬眠相关的近乎完全脑缺血的耐受性。
