Hemond P, Jaffe D B
Department of Biology, University of Texas at San Antonio, San Antonio, TX 78249, USA.
Neuroscience. 2005;135(2):413-20. doi: 10.1016/j.neuroscience.2005.05.044.
In hippocampal pyramidal neurons from aged animals voltage-gated Ca2+ entry and the slow, post-burst afterhyperpolarization are enhanced. As a result, there is a decrease in neuronal excitability and, in turn, an alteration in synaptic plasticity. Restricting the caloric intake of a rodent is a well-known paradigm for increasing lifespan and ameliorating a number of neurodegenerative features of aging, including deficits in synaptic plasticity and cognition. Here we show in rat CA1 pyramidal neurons from aged animals (18-20 months old) that a restricted diet prevents the enhancement of dendritic spike-mediated Ca2+ accumulation. In contrast, no significant changes in the rates of Ca2+ recovery were observed suggesting that Ca2+ clearance mechanisms are not affected by aging or caloric restriction. Lastly, we found that caloric restriction also prevented the aging-associated increase in the slow, post-burst afterhyperpolarization. Our results suggest that caloric restriction-sensitive changes in Ca2+ accumulation and membrane excitability may in part account for the protective effects of dietary restriction on synaptic plasticity and learning deficits in aged animals.
在老年动物的海马锥体神经元中，电压门控性Ca2+内流以及爆发后缓慢的超极化增强。结果，神经元兴奋性降低，进而导致突触可塑性改变。限制啮齿动物的热量摄入是一种众所周知的延长寿命和改善衰老的许多神经退行性特征的范例，包括突触可塑性和认知缺陷。在这里，我们在老年动物（18 - 20个月大）的大鼠CA1锥体神经元中发现，限制饮食可防止树突棘介导的Ca2+积累增强。相比之下，未观察到Ca2+恢复速率的显著变化，这表明Ca2+清除机制不受衰老或热量限制的影响。最后，我们发现热量限制还可防止与衰老相关的爆发后缓慢超极化增加。我们的结果表明，Ca2+积累和膜兴奋性中对热量限制敏感的变化可能部分解释了饮食限制对老年动物突触可塑性和学习缺陷的保护作用。
