γ-氨基丁酸B型(GABA(B))受体在人类运动皮层皮质内抑制中的作用。
The role of GABA(B) receptors in intracortical inhibition in the human motor cortex.
作者信息
McDonnell Michelle N, Orekhov Yuri, Ziemann Ulf
机构信息
Research Centre for Human Movement Control, The University of Adelaide, Adelaide, Australia.
出版信息
Exp Brain Res. 2006 Aug;173(1):86-93. doi: 10.1007/s00221-006-0365-2. Epub 2006 Feb 18.
While GABA(B) receptors are thought to have an important role in mediating long interval intracortical inhibition (LICI) in the human motor cortex, the effect of a selective GABA(B) receptor agonist on this measure has not been directly tested. Nine healthy volunteers ingested either 50 mg baclofen (BAC) or placebo (PBO) in a randomized, double blind crossover design, with the second session one week later. We used transcranial magnetic stimulation to assess motor threshold, motor evoked potential (MEP) amplitude, cortical silent period (CSP) duration, short interval intracortical inhibition (SICI) and LICI before and 90 min following drug intake. There was no specific effect of drug on motor threshold, MEP amplitude or CSP duration. BAC resulted in a significant increase in LICI (P=0.002) and a significant decrease in SICI (P=0.046) while PBO had no effect. Our findings demonstrate that the enhanced GABA(B) receptor activation results in differential effects on these two measures of intracortical inhibition in the human motor cortex. The increase in LICI is likely to be a result of increased GABA(B) receptor mediated inhibitory post-synaptic potentials, while the reduction in SICI may relate to the activation of pre-synaptic GABA(B) receptors reducing GABA release.
虽然γ-氨基丁酸B(GABA(B))受体被认为在介导人类运动皮层的长时程皮质内抑制(LICI)中起重要作用,但选择性GABA(B)受体激动剂对该指标的影响尚未得到直接测试。9名健康志愿者按照随机、双盲交叉设计摄入50毫克巴氯芬(BAC)或安慰剂(PBO),一周后进行第二阶段测试。我们在药物摄入前及摄入后90分钟,使用经颅磁刺激来评估运动阈值、运动诱发电位(MEP)幅度、皮质静息期(CSP)时长、短时程皮质内抑制(SICI)和LICI。药物对运动阈值、MEP幅度或CSP时长没有特定影响。BAC使LICI显著增加(P = 0.002),使SICI显著降低(P = 0.046),而PBO则无作用。我们的研究结果表明,增强的GABA(B)受体激活对人类运动皮层的这两种皮质内抑制指标产生不同影响。LICI的增加可能是GABA(B)受体介导的抑制性突触后电位增加的结果,而SICI的降低可能与突触前GABA(B)受体激活减少GABA释放有关。