School of Biomedical Engineering, McMaster University, Hamilton, Ontario, Canada.
Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
J Physiol. 2024 May;602(10):2253-2264. doi: 10.1113/JP286126. Epub 2024 Apr 18.
Short- and long-latency afferent inhibition (SAI and LAI respectively) are phenomenon whereby the motor evoked potential induced by transcranial magnetic stimulation (TMS) is inhibited by a sensory afferent volley consequent to nerve stimulation. It remains unclear whether dopamine participates in the genesis or modulation of SAI and LAI. The present study aimed to determine if SAI and LAI are modulated by levodopa (l-DOPA). In this placebo-controlled, double-anonymized study Apo-Levocarb (100 mg l-DOPA in combination with 25 mg carbidopa) and a placebo were administered to 32 adult males (mean age 24 ± 3 years) in two separate sessions. SAI and LAI were evoked by stimulating the median nerve and delivering single-pulse TMS over the motor hotspot corresponding to the first dorsal interosseous muscle of the right hand. SAI and LAI were quantified before and 1 h following ingestion of drug or placebo corresponding to the peak plasma concentration of Apo-Levocarb. The results indicate that Apo-Levocarb increases SAI and does not significantly alter LAI. These findings support literature demonstrating increased SAI following exogenous dopamine administration in neurodegenerative disorders. KEY POINTS: Short- and long-latency afferent inhibition (SAI and LAI respectively) are measures of corticospinal excitability evoked using transcranial magnetic stimulation. SAI and LAI are reduced in conditions such as Parkinson's disease which suggests dopamine may be involved in the mechanism of afferent inhibition. 125 mg of Apo-Levocarb (100 mg dopamine) increases SAI but not LAI. This study increases our understanding of the pharmacological mechanism of SAI and LAI.
短潜伏期和长潜伏期传入抑制(分别为 SAI 和 LAI)是一种现象,即在经颅磁刺激(TMS)诱导的运动诱发电位被随后的神经刺激引起的感觉传入冲动所抑制。多巴胺是否参与 SAI 和 LAI 的产生或调节尚不清楚。本研究旨在确定左旋多巴(l-DOPA)是否调节 SAI 和 LAI。在这项安慰剂对照、双盲研究中,32 名成年男性(平均年龄 24 ± 3 岁)在两个单独的时段分别接受了 Apo-Levocarb(100mg l-DOPA 与 25mg 卡比多巴的组合)和安慰剂治疗。通过刺激正中神经并在手的第一背侧骨间肌的运动热点上施加单脉冲 TMS 来诱发 SAI 和 LAI。在服用药物或安慰剂后 1 小时内,即在 Apo-Levocarb 的峰值血浆浓度时,测量 SAI 和 LAI。结果表明,Apo-Levocarb 增加了 SAI,但对 LAI 没有显著影响。这些发现支持了在外源性多巴胺给药后增加 SAI 的文献报道。要点:短潜伏期和长潜伏期传入抑制(分别为 SAI 和 LAI)是使用经颅磁刺激诱发的皮质脊髓兴奋性的测量。SAI 和 LAI 在帕金森病等情况下会降低,这表明多巴胺可能参与传入抑制的机制。125mg 的 Apo-Levocarb(100mg 多巴胺)增加了 SAI,但没有增加 LAI。这项研究增加了我们对 SAI 和 LAI 的药理学机制的理解。