Schmidt Annika, Meindl Tobias, Albu-Schäffer Alin, Franklin David W, Stratmann Philipp
TUM School of Computation, Information and Technology, Technical University of Munich (TUM), 85748, Garching, Germany.
Institute of Robotics and Mechtronics, German Aerospace Center (DLR), 82234, Wessling, Germany.
Sci Rep. 2025 May 13;15(1):16588. doi: 10.1038/s41598-025-00444-1.
Neuromodulation plays a central role in human movement control. An imbalance of neurotransmitters, especially dopamine and serotonin, can be associated with various neurological disorders causing tremors or spasms. Specifically, serotonin was shown to scale motoneuron excitability following intense muscle contractions, affecting short-latency reflexes. Likely, it may also influence motoneuron modulation in prolonged contractions, although this lacks experimental evidence. An intriguing test case for this hypothesis is presented by the Kohnstamm phenomenon, where sustained muscle contractions lead to prolonged amplified EMG activity and involuntary motions, aligning with the timescale of serotonergic amplification. The suspected serotonin influence on this effect was tested in a placebo-controlled human user study with 14 participants, where half were administered the serotonin antagonist Cyproheptadine and the other half a placebo. Comparing EMG and force responses after inducing the Kohnstamm phenomenon in the deltoid muscles revealed statistically significant faster EMG decay with the serotonin antagonist, while decay remained consistent in the placebo group compared to the response of the same participant group without medication. The force measurements showed the same trend, although no significance. This provides new data-based evidence that serotonin contributes to long-term motoneuron modulation, extending previous findings about the dedicated role and influence of this neurotransmitter. Additionally, the work suggests the phenomenon as an interesting test case to investigate the dedicated involvement of different neurocontrol mechanisms such as Persistent Inward Currents.
神经调节在人体运动控制中起着核心作用。神经递质失衡，尤其是多巴胺和血清素失衡，可能与导致震颤或痉挛的各种神经系统疾病有关。具体而言，血清素在剧烈肌肉收缩后可调节运动神经元兴奋性，影响短潜伏期反射。虽然缺乏实验证据，但在长时间收缩中血清素也可能影响运动神经元调节。科恩斯塔姆现象为此假设提供了一个有趣的测试案例，在该现象中，持续的肌肉收缩会导致肌电图活动延长放大和不自主运动，这与血清素能放大的时间尺度一致。在一项有14名参与者的安慰剂对照人体用户研究中，测试了血清素对这种效应的潜在影响，其中一半参与者服用血清素拮抗剂赛庚啶，另一半服用安慰剂。比较三角肌诱发科恩斯塔姆现象后的肌电图和力量反应发现，服用血清素拮抗剂后肌电图衰减在统计学上显著更快，而与未用药的同一参与者组的反应相比，安慰剂组的衰减保持一致。力量测量显示了相同趋势，尽管不显著。这提供了基于新数据的证据，证明血清素有助于长期运动神经元调节，扩展了先前关于这种神经递质的特定作用和影响的研究结果。此外，这项研究表明该现象是一个有趣的测试案例，可用于研究不同神经控制机制（如持续性内向电流）的特定参与情况。
