Human motoneurone excitability is depressed by activation of serotonin 1A receptors with buspirone

J. D’Amico, A. Butler, M. Héroux, Florence Cotel, J. Perrier, J. Butler, S. Gandevia, Janet L. Taylor
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引用次数: 26

Abstract

In the adult turtle spinal cord, action potential generation in motoneurones is inhibited by spillover of serotonin to extrasynaptic serotonin 1A (5‐HT1A) receptors at the axon initial segment. We explored whether ingestion of the 5‐HT1A receptor partial agonist, buspirone, decreases motoneurone excitability in humans. Following ingestion of buspirone, two tests of motoneurone excitability showed decreases. F‐wave areas and persistence in an intrinsic muscle of the hand were reduced, as was the area of cervicomedullary motor evoked potentials in biceps brachii. Our findings suggest that activation of 5‐HT1A receptors depresses human motoneurone excitability. Such a depression could contribute to decreased motoneurone output during fatiguing exercise if there is high serotonergic drive to the motoneurones.
丁螺环酮激活5 -羟色胺1A受体可抑制人运动神经元的兴奋性
在成年海龟脊髓中,运动神经元的动作电位产生被5 -羟色胺溢出到轴突初始段的突触外5 -羟色胺1A(5‐HT1A)受体所抑制。我们研究了摄入5‐HT1A受体部分激动剂丁螺环酮是否会降低人类运动神经元的兴奋性。服用丁螺环酮后,运动神经元兴奋性的两项测试显示下降。手部固有肌肉的F波区域和持续时间减少,肱二头肌的颈髓运动诱发电位区域也减少。我们的研究结果表明,5‐HT1A受体的激活会抑制人类运动神经元的兴奋性。如果运动神经元受到高血清素的驱动,这种抑郁可能会导致疲劳运动时运动神经元输出减少。
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