Pitler T A, Landfield P W
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27103.
Brain Res. 1990 Jan 29;508(1):1-6. doi: 10.1016/0006-8993(90)91109-t.
Calcium (Ca) spike potentials were investigated in cesium-loaded, tetrodotoxin (TTX)-treated CA1 pyramidal cells in hippocampal slices from young-mature and aged rats. The duration of single Ca spike potentials was prolonged in cells from aged rats, indicating that previously observed age-related changes in Ca-dependent mechanisms (e.g. in the K-mediated afterhyperpolarization and in frequency potentiation) may result from an age-related increase of voltage-dependent Ca conductance. Since we recently found that Ca spike duration in hippocampus can be modulated strongly by a form of Ca-dependent inactivation of Ca current, spike inactivation paradigms also were examined. However, following 5- or 10-s-long depolarizing pulses, or during a 2-Hz train of elicited Ca spikes, there were no age differences in percent inactivation. These results do not support (but do not fully rule out) the possibility that impaired Ca-dependent inactivation underlies the increase in the Ca spike with aging. Conceivably, this prolongation of voltage-dependent Ca influx could have implications for our understanding of normal and abnormal brain aging.
在来自年轻成熟和老年大鼠的海马切片中，对用铯负载并经河豚毒素（TTX）处理的CA1锥体神经元中的钙（Ca）峰电位进行了研究。老年大鼠细胞中单个钙峰电位的持续时间延长，这表明先前观察到的与年龄相关的钙依赖性机制变化（例如钾介导的超极化后电位和频率增强）可能是由于电压依赖性钙电导随年龄增长而增加所致。由于我们最近发现海马体中的钙峰持续时间可通过一种钙电流的钙依赖性失活形式进行强烈调节，因此也研究了峰失活模式。然而，在5秒或10秒的去极化脉冲后，或在2赫兹的诱发钙峰串期间，失活百分比没有年龄差异。这些结果不支持（但也没有完全排除）钙依赖性失活受损是衰老过程中钙峰增加的基础这一可能性。可以想象，这种电压依赖性钙内流的延长可能会影响我们对正常和异常脑衰老的理解。
