University of Miami, Department of Neurological Surgery, The Miami Project to Cure Paralysis, Miami, FL, 33136, USA.
Bruce W. Carter Department of Veterans Affairs Medical Centre, 1201 NW 16th Street, Miami, FL, 33125, USA.
J Physiol. 2017 Sep 15;595(18):6203-6217. doi: 10.1113/JP274504. Epub 2017 Aug 18.
It has long been known that the somatosensory cortex gates sensory inputs from the contralateral side of the body. Here, we examined the contribution of the ipsilateral somatosensory cortex (iS1) to sensory gating during index finger voluntary activity. The amplitude of the P25/N33, but not other somatosensory evoked potential (SSEP) components, was reduced during voluntary activity compared with rest. Interhemispheric inhibition between S1s and intracortical inhibition in the S1 modulated the amplitude of the P25/N33. Note that changes in interhemispheric inhibition between S1s correlated with changes in cortical circuits in the ipsilateral motor cortex. Our findings suggest that cortical circuits, probably from somatosensory and motor cortex, contribute to sensory gating in the iS1 during voluntary activity in humans.
An important principle in the organization of the somatosensory cortex is that it processes afferent information from the contralateral side of the body. The role of the ipsilateral somatosensory cortex (iS1) in sensory gating in humans remains largely unknown. Using electroencephalographic (EEG) recordings over the iS1 and electrical stimulation of the ulnar nerve at the wrist, we examined somatosensory evoked potentials (SSEPs; P14/N20, N20/P25 and P25/N33 components) and paired-pulse SSEPs between S1s (interhemispheric inhibition) and within (intracortical inhibition) the iS1 at rest and during tonic index finger voluntary activity. We found that the amplitude of the P25/N33, but not other SSEP components, was reduced during voluntary activity compared with rest. Interhemispheric inhibition increased the amplitude of the P25/N33 and intracortical inhibition reduced the amplitude of the P25/N33, suggesting a cortical origin for this effect. The P25/N33 receives inputs from the motor cortex, so we also examined the contribution of distinct sets of cortical interneurons by testing the effect of ulnar nerve stimulation on motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation over the ipsilateral motor cortex with the coil in the posterior-anterior (PA) and anterior-posterior (AP) orientation. Afferent input attenuated PA, but not AP, MEPs during voluntary activity compared with rest. Notably, changes in interhemispheric inhibition correlated with changes in PA MEPs. Our novel findings suggest that interhemispheric projections between S1s and intracortical circuits, probably from somatosensory and motor cortex, contribute to sensory gating in the iS1 during voluntary activity in humans.
长期以来，人们一直知道躯体感觉皮层对来自身体对侧的感觉输入进行门控。在这里，我们研究了在食指自愿活动期间，对侧躯体感觉皮层（iS1）对感觉门控的贡献。与休息相比，P25/N33 的幅度在自愿活动期间减少，但其他体感诱发电位（SSEP）成分则没有。S1 之间的半球间抑制和 S1 内的皮质内抑制调节 P25/N33 的幅度。请注意，S1 之间的半球间抑制的变化与对侧运动皮层中的皮质回路的变化相关。我们的发现表明，皮质回路可能来自躯体感觉和运动皮层，有助于人类在自愿活动期间 iS1 中的感觉门控。
躯体感觉皮层组织的一个重要原则是，它处理来自身体对侧的传入信息。人类对侧躯体感觉皮层（iS1）在感觉门控中的作用在很大程度上仍不清楚。我们使用脑电图（EEG）记录 iS1 上的记录和腕部尺神经的电刺激，在静息和紧张的食指自愿活动期间，我们检查了体感诱发电位（SSEPs；P14/N20、N20/P25 和 P25/N33 成分）和 S1 之间的成对脉冲 SSEPs（半球间抑制）和 iS1 内（皮质内抑制）。我们发现，与休息相比，P25/N33 的幅度在自愿活动期间减少，但其他 SSEP 成分则没有。半球间抑制增加了 P25/N33 的幅度，皮质内抑制降低了 P25/N33 的幅度，这表明这种效应的皮质起源。P25/N33 接收来自运动皮层的输入，因此我们还通过测试尺神经刺激对经颅磁刺激在对侧运动皮层上诱发的运动诱发电位（MEPs）的影响，研究了不同皮质中间神经元集的贡献，线圈在前后（PA）和前-后（AP）方向。与休息相比，与自愿活动相比，传入输入减弱了 PA，但没有减弱 AP 的 MEPs。值得注意的是，半球间抑制的变化与 PA MEPs 的变化相关。我们的新发现表明，S1 之间的半球间投射和皮质内回路，可能来自躯体感觉和运动皮层，有助于人类在自愿活动期间 iS1 中的感觉门控。
