Kaelin-Lang Alain, Luft Andreas R, Sawaki Lumy, Burstein Aaron H, Sohn Young H, Cohen Leonardo G
Human Cortical Physiology Section, NINDS, National Institutes of Health, Bethesda, MD 20892, USA.
J Physiol. 2002 Apr 15;540(Pt 2):623-33. doi: 10.1113/jphysiol.2001.012801.
In humans, somatosensory stimulation results in increased corticomotoneuronal excitability to the stimulated body parts. The purpose of this study was to investigate the underlying mechanisms. We recorded motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) from abductor pollicis brevis (APB), first dorsal interosseous (FDI), and abductor digiti minimi (ADM) muscles. MEP amplitudes, recruitment curves (RC), intracortical inhibition (ICI), intracortical facilitation (ICF), resting (rMT) and active motor thresholds (aMT) were recorded before and after a 2-h period of ulnar nerve electrical stimulation at the wrist. Somatosensory input was monitored by recording somatosensory evoked potentials. To differentiate excitability changes at cortical vs. subcortical sites, we recorded supramaximal peripheral M-responses and MEPs to brainstem electrical stimulation (BES). In order to investigate the involvement of GABAergic mechanisms, we studied the influence of lorazepam (LZ) (a GABA(A) receptor agonist) relative to that of dextromethorphan (DM) (an NMDA receptor antagonist) and placebo in a double-blind design. We found that somatosensory stimulation increased MEP amplitudes to TMS only in the ADM, confirming a previous report. This effect was blocked by LZ but not by either DM or placebo and lasted between 8 and 20 min in the absence of (i) changes in MEPs elicited by BES, (ii) amplitudes of early somatosensory-evoked potentials or (iii) M-responses. We conclude that somatosensory stimulation elicited a focal increase in corticomotoneuronal excitability that outlasts the stimulation period and probably occurs at cortical sites. The antagonistic effect of LZ supports the hypothesis of GABAergic involvement as an operating mechanism.
在人类中，体感刺激会导致对受刺激身体部位的皮质运动神经元兴奋性增加。本研究的目的是探究其潜在机制。我们记录了来自拇短展肌（APB）、第一背侧骨间肌（FDI）和小指展肌（ADM）肌肉对经颅磁刺激（TMS）的运动诱发电位（MEP）。在手腕处进行2小时尺神经电刺激前后，记录MEP波幅、募集曲线（RC）、皮质内抑制（ICI）、皮质内易化（ICF）、静息（rMT）和主动运动阈值（aMT）。通过记录体感诱发电位来监测体感输入。为了区分皮质与皮质下部位的兴奋性变化，我们记录了最大外周M反应和对脑干电刺激（BES）的MEP。为了研究GABA能机制的参与情况，我们在双盲设计中研究了劳拉西泮（LZ）（一种GABA(A)受体激动剂）相对于右美沙芬（DM）（一种NMDA受体拮抗剂）和安慰剂的影响。我们发现，体感刺激仅增加了ADM对TMS的MEP波幅，这证实了之前的一份报告。这种效应被LZ阻断，但未被DM或安慰剂阻断，并且在不存在以下情况时持续8至20分钟：（i）BES诱发的MEP变化；（ii）早期体感诱发电位的波幅；或（iii）M反应。我们得出结论，体感刺激引起皮质运动神经元兴奋性的局部增加，这种增加在刺激期后仍持续存在，并且可能发生在皮质部位。LZ的拮抗作用支持了GABA能参与作为一种作用机制的假说。
