Department of Clinical Neurophysiology, University Medical Centre Göttingen, Göttingen, Germany.
Medical Research Division, National Research Center, Cairo, Egypt.
J Neurophysiol. 2021 Jul 1;126(1):340-348. doi: 10.1152/jn.00065.2021. Epub 2021 Jun 30.
During transcranial electric stimulation, increasing intracellular Ca levels beyond those needed for inducing long term potentiation (LTP) may collapse aftereffects. State-dependent plastic aftereffects are reduced when applied during muscle activation as compared with rest. Cortical surround inhibition by antagonistic muscle activation inhibits the center-innervated agonist. The objective of this study is to determine the interaction of state dependency of transcranial alternating current stimulation (tACS) aftereffects at rest and under activation of agonist and antagonist muscles during stimulation with different intensities. In 13 healthy participants, we measured motor-evoked potential (MEP) amplitudes before and after applying tACS at 140 Hz over the motor cortex in nine single-blinded sessions using sham, 1 mA, and 2 mA stimulation intensities during rest and activation of agonist and antagonist muscles. During rest, only 1 mA tACS produced a significant MEP increase, whereas the 2 mA stimulation produced no significant MEP size shift. During agonist activation 1 mA did not induce MEP changes; after 2 mA, first a decrease and later an increase of MEPs were observed. Antagonist activation under sham tACS led to an inhibition, which was restored to baseline by 1 and 2 mA tACS. Increasing stimulation intensity beyond 1 mA does not increase excitability, compatible with too strong intracellular Ca increase. Antagonist innervation leads to MEP inhibition, supporting the concept of surround inhibition, which can be overcome by tACS at both intensities. During agonist innervation, a tACS dose-dependent relationship exists. Our results integrate concepts of "leaky membranes" under activation, surround inhibition, intracellular Ca increase, and their role in the aftereffects of tACS. Stimulation intensity and activation of center versus surround muscles affect cortical excitability alterations generated by 140-Hz tACS. At rest, excitatory aftereffects were induced by tACS with 1 mA, but not 2 mA stimulation intensity. With agonistic muscle activation, excitability first decreases, and then increases with 2 mA. For antagonist activation, the MEP amplitude reduction observed in the sham condition is counteracted upon by 1 and 2 mA tACS. This reflects the relation of LTP-like aftereffects to Ca concentration alterations.
在经颅电刺激过程中,细胞内 Ca 水平的增加超过诱导长时程增强 (LTP) 所需的水平可能会导致后效崩溃。与休息时相比,在肌肉激活期间施加依赖状态的塑性后效会降低。拮抗肌激活引起的皮层环绕抑制抑制中心支配的激动剂。本研究的目的是确定在不同强度刺激下,静息状态下和激动剂和拮抗剂肌肉激活时,经颅交流电刺激 (tACS) 后效的状态依赖性相互作用。在 13 名健康参与者中,我们在 9 个单盲会话中使用假刺激、1 mA 和 2 mA 刺激强度,在运动皮层上以 140 Hz 施加 tACS 前后测量运动诱发电位 (MEP) 幅度,在静息和激动剂和拮抗剂肌肉激活期间。在静息状态下,只有 1 mA 的 tACS 产生了显著的 MEP 增加,而 2 mA 的刺激没有产生显著的 MEP 大小变化。在激动剂激活时,1 mA 没有引起 MEP 变化;在 2 mA 后,首先观察到 MEP 的减少,然后是增加。假刺激下的拮抗剂激活导致抑制,1 mA 和 2 mA 的 tACS 可将其恢复到基线。增加刺激强度超过 1 mA 不会增加兴奋性,这与细胞内 Ca 增加过强一致。拮抗剂神经支配导致 MEP 抑制,支持环绕抑制的概念,这可以通过两种强度的 tACS 克服。在激动剂神经支配下,存在 tACS 剂量依赖性关系。我们的结果整合了激活下“漏膜”、环绕抑制、细胞内 Ca 增加及其在 tACS 后效中的作用的概念。刺激强度和中心与周围肌肉的激活会影响 140 Hz tACS 产生的皮质兴奋性改变。在静息状态下,1 mA 的 tACS 可产生兴奋性后效,但 2 mA 的刺激强度不行。在激动剂肌肉激活下,兴奋性首先降低,然后随着 2 mA 的增加而增加。对于拮抗剂激活,在假状态下观察到的 MEP 幅度减少被 1 mA 和 2 mA 的 tACS 抵消。这反映了 LTP 样后效与 Ca 浓度变化的关系。