Faculty of Health Sciences, University of Ontario Institute of Technology, 2000 Simcoe St. North, Oshawa, Ontario, Canada.
J Physiol. 2010 Aug 1;588(Pt 15):2839-57. doi: 10.1113/jphysiol.2010.188722. Epub 2010 Jun 14.
This is the first study to report on the increase in motoneurone excitability during fictive scratch in adult decerebrate cats. Intracellular recordings from antidromically identified motoneurones revealed a decrease in the voltage threshold for spike initiation (V(th)), a suppression of motoneurone afterhyperpolarization and activation of voltage-dependent excitation at the onset of scratch. These state-dependent changes recovered within 10-20 s after scratch and could be evoked after acute transection of the spinal cord at C1. Thus, there is a powerful intraspinal system that can quickly and reversibly re-configure neuronal excitability during spinal network activation. Fictive scratch was evoked in spinal intact and transected decerebrate preparations by stroking the pinnae following topical curare application to the dorsal cervical spinal cord and neuromuscular block. Hyperpolarization of V(th) occurred (mean 5.8 mV) in about 80% of ipsilateral flexor, extensor or bifunctional motoneurones during fictive scratch. The decrease in V(th) began before any scratch-evoked motoneurone activity as well as during the initial phase in which extensors are tonically hyperpolarized. The V(th) of contralateral extensors depolarized by a mean of +3.7 mV during the tonic contralateral extensor activity accompanying ipsilateral scratch. There was a consistent and substantial reduction of afterhyperpolarization amplitude without large increases in motoneurone conductance in both spinal intact and transected preparations. Depolarizing current injection increased, and hyperpolarization decreased the amplitude of rhythmic scratch drive potentials in acute spinal preparations indicating that the spinal scratch-generating network can activate voltage-dependent conductances in motoneurones. The enhanced excitability in spinal preparations associated with fictive scratch indicates the existence of previously unrecognized, intraspinal mechanisms increasing motoneurone excitability.
这是第一项关于在去大脑成年猫的虚构抓挠过程中运动神经元兴奋性增加的研究。对顺行性识别的运动神经元进行细胞内记录显示，其锋电位起始电压阈值 (V(th)) 降低，运动神经元后超极化抑制，以及在抓挠开始时激活电压依赖性兴奋。这些状态依赖的变化在抓挠后 10-20 秒内恢复，并且可以在 C1 处急性切断脊髓后诱发。因此，在脊髓网络激活期间，存在一种强大的脊髓内系统，可以快速且可逆地重新配置神经元兴奋性。在脊髓完整和脊髓切断去大脑制剂中，通过在向背侧颈脊髓表面施用箭毒后刷动耳郭来诱发虚构抓挠和神经肌肉阻滞。在虚构抓挠期间，约 80%的同侧屈肌、伸肌或双功能运动神经元的 V(th)发生超极化（平均 5.8 mV）。V(th) 的降低发生在任何虚构抓挠诱发的运动神经元活动之前，以及在伸展肌持续去极化的初始阶段。在伴随同侧抓挠的持续对侧伸肌活动期间，对侧伸肌的 V(th)平均向正方向去极化+3.7 mV。在脊髓完整和切断的制剂中，在后超极化幅度没有明显增加的情况下，后超极化幅度有一致且实质性的降低。在急性脊髓制剂中，去极化电流注入增加，超极化降低节律性抓挠驱动电位的幅度，表明脊髓抓挠产生网络可以激活运动神经元中的电压依赖性电导。与虚构抓挠相关的脊髓制剂的兴奋性增强表明存在以前未被认识的、脊髓内机制增加运动神经元兴奋性。
