Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
J Neurophysiol. 2021 Apr 1;125(4):1269-1278. doi: 10.1152/jn.00673.2020. Epub 2021 Feb 24.
Although ynaptic transmission in motor pathways can be regulated by neuromodulators, such as acetylcholine, few studies have examined how cholinergic activity affects cortical and spinal motor circuits following muscle contractions of varying intensities. This was a human, double-blinded, placebo-controlled, crossover study. Participants attended two sessions where they were administered either a placebo or 25 mg of promethazine. Electromyography of the abductor digiti minimi (ADM) was measured for all conditions. Motor evoked potentials (MEPs) were obtained via motor cortical transcranial magnetic stimulation (TMS), and F waves were obtained via ulnar nerve electrical stimulation. MEPs and F waves were examined: ) when the muscle was at rest; ) after the muscle had been active; and ) after the muscle had been fatigued. MEPs were unaffected by muscarinic receptor blockade when measurements were recorded from resting muscle or following a 50% isometric maximal voluntary contraction (MVC). However, muscarinic receptor blockade increased MEP area following a 10-s MVC ( = 0.019) and following a fatiguing 60-s MVC ( = 0.040). F wave area and persistence were not affected by promethazine for any muscle contraction condition. Corticospinal excitability was influenced by cholinergic effects when voluntary drive to the muscle was high. Given that spinal motoneurone excitability remained unaffected, it is likely that cholinergic effects are influential within the motor cortex during strong muscle contractions. Future research should evaluate how cholinergic effects alter the relationship between subcortical structures and the motor cortex, as well as brainstem neuromodulatory pathways and spinal motoneurons. The relationship between motor function and cholinergic circuitry in the central nervous system is complex. Although many studies have approached this issue at the cellular level, few studies have examined cholinergic mechanisms in humans performing muscle contractions. This study demonstrates that blockade of muscarinic acetylcholine receptors enhances motor evoked potentials (elicited with transcranial magnetic stimulation) following strong muscle contractions, but not weak muscle contractions.
虽然运动通路中的突触传递可以被神经调质（如乙酰胆碱）调节，但很少有研究探讨胆碱能活性如何影响不同强度肌肉收缩后的皮质和脊髓运动回路。这是一项在人类中进行的、双盲、安慰剂对照、交叉研究。参与者参加了两次会议，在会议中他们接受了安慰剂或 25 毫克苯海拉明的治疗。对小指展肌（ADM）的肌电图进行了所有条件下的测量。通过运动皮质经颅磁刺激（TMS）获得运动诱发电位（MEP），通过尺神经电刺激获得 F 波。检查了 MEP 和 F 波：）在肌肉静止时；）在肌肉活动后；）在肌肉疲劳后。当从休息的肌肉或在进行 50%等长最大自主收缩（MVC）后进行测量时，毒蕈碱受体阻断对 MEP 区域没有影响。然而，毒蕈碱受体阻断增加了 10 秒 MVC 后的 MEP 区域（=0.019）和疲劳 60 秒 MVC 后的 MEP 区域（=0.040）。在任何肌肉收缩条件下，F 波区域和持续时间均不受苯海拉明影响。当肌肉的自主驱动较高时，皮质脊髓兴奋性受到胆碱能作用的影响。鉴于脊髓运动神经元兴奋性不受影响，因此在强烈的肌肉收缩期间，胆碱能作用很可能在运动皮质内发挥作用。未来的研究应评估胆碱能作用如何改变下皮层结构与运动皮层之间的关系，以及脑干神经调质途径和脊髓运动神经元之间的关系。运动功能与中枢神经系统中的胆碱能回路之间的关系很复杂。尽管许多研究在细胞水平上探讨了这个问题，但很少有研究在进行肌肉收缩的人类中检查胆碱能机制。本研究表明，毒蕈碱乙酰胆碱受体阻断增强了强肌肉收缩后的运动诱发电位（经颅磁刺激诱发），但对弱肌肉收缩没有影响。
