Altered neural excitability is considered a prominent contributing factor to cognitive decline during aging. A clear example is the excess neural activity observed in several temporal lobe structures of cognitively impaired older individuals in rodents and humans. At a cellular level, aging-related changes in mechanisms regulating intrinsic excitability have been well examined in pyramidal cells of the CA1 hippocampal subfield. Studies in the inbred Fisher 344 rat strain document an age-related increase in the slow afterhyperpolarization (AHP) that normally occurs after a burst of action potentials, and serves to reduce subsequent firing. We evaluated the status of the AHP in the outbred Long-Evans rat, a well-established model for studying individual differences in neurocognitive aging. In contrast to the findings reported in the Fisher 344 rats, in the Long-Evan rats we detected a selective reduction in AHP in cognitively impaired aged individuals. We discuss plausible scenarios to account for these differences and also discuss possible implications of these differences.

中文翻译：

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以个体差异为特征的老年 Long-Evans 大鼠 Ca1 锥体细胞的超极化后振幅

改变的神经兴奋性被认为是导致衰老过程中认知能力下降的重要因素。一个明显的例子是在啮齿动物和人类认知障碍老年人的几个颞叶结构中观察到的过度神经活动。在细胞水平上，已经在 CA1 海马亚区的锥体细胞中很好地检查了调节内在兴奋性机制中与衰老相关的变化。对近交系 Fisher 344 大鼠品系的研究记录了与年龄相关的缓慢后超极化 (AHP) 的增加，这通常发生在动作电位爆发后，并有助于减少随后的放电。我们评估了远交的 Long-Evans 大鼠的 AHP 状态，这是一种成熟的模型，用于研究神经认知衰老的个体差异。与 Fisher 344 大鼠报告的结果相反，在 Long-Evan 大鼠中，我们检测到认知障碍老年人的 AHP 选择性降低。我们讨论了解释这些差异的合理场景，并讨论了这些差异的可能影响。