Sarcopenia, or pathological age-related loss of muscle strength and mass, contributes to physical function impairment in older adults. While current understanding of sarcopenia is centered mostly on neuromuscular mechanisms, mounting evidence supports that deficits at the level of the primary motor cortex (PMC) play a significant role. Despite the importance of the PMC to initiate movement, understanding of how age affects the excitability of layer V pyramidal neurons (LVPNs) of the PMC is limited. To address this, we used the whole-cell patch clamp technique to measure the excitability of LVPNs of the PMC in young, late adulthood, and old mice. Old LVPNs had increased firing frequency and membrane input resistance, but no differences in action potential kinetics versus young and late adulthood mice. Since changes in the persistent inward current (PIC) are known to contribute to changes in motor neuron excitability, we measured LVPN PICs as a putative contributor to LVPN excitability. The PIC amplitude was increased in old LVPN via increases in Na⁺ and Ca²⁺ PICs, in addition to being active across a wider voltage range. Given that LVPN function is integral to initiation of voluntary muscle contraction, altered LVPN excitability likely contributes to age-related impairment of physical function.

肌肉减少症或病理性年龄相关的肌肉力量和质量丧失，会导致老年人的身体功能受损。虽然目前对肌肉减少症的理解主要集中在神经肌肉机制上，但越来越多的证据支持初级运动皮层 （PMC） 水平的缺陷起着重要作用。尽管 PMC 对启动运动很重要，但对年龄如何影响 PMC 第 V 层锥体神经元 （LVPN） 兴奋性的理解是有限的。为了解决这个问题，我们使用全细胞膜片钳技术来测量 PMC 的 LVPNs 在年轻、成年晚期和老年小鼠中的兴奋性。老年 LVPN 的放电频率和膜输入电阻增加，但与年轻和成年晚期小鼠相比，动作电位动力学没有差异。由于已知持续向内电流 （PIC） 的变化会导致运动神经元兴奋性的变化，因此我们测量了 LVPN PIC 作为 LVPN 兴奋性的推定贡献者。在旧 LVPN 中，除了在更宽的电压范围内处于活动状态外，还通过增加 Na⁺ 和 Ca²⁺ PIC 来增加 PIC 幅度。鉴于 LVPN 功能是随意肌收缩启动不可或缺的一部分，LVPN 兴奋性的改变可能导致与年龄相关的身体机能损害。