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首页> 外文期刊>The Journal of Physiology >Immobilization induces changes in presynaptic control of group Ia afferents in healthy humans.
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Immobilization induces changes in presynaptic control of group Ia afferents in healthy humans.

机译:固定诱导健康人中Ia组传入神经突触前控制的改变。

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Neural plasticity occurs throughout adult life in response to maturation, use and disuse. Recent studies have documented that H-reflex amplitudes increase following a period of immobilization. To elucidate the mechanisms contributing to the increase in H-reflex size following immobilization we immobilized the left foot and ankle joint for 2 weeks in 12 able-bodied subjects. Disynaptic reciprocal inhibition of soleus (SOL) motoneurons and presynaptic control of SOL group Ia afferents was measured before and after the immobilization as well as following 2 weeks of recovery. Following immobilization, maximal voluntary plantar- and dorsiflexion torque (MVC) was significantly reduced and the maximal SOL H-reflex amplitude increased with no changes in the maximal compound motor response (M(max)). Decreased presynaptic inhibition of the Ia afferents probably contributed to the increase of the H-reflex size, since we observed a significant decrease in the long-latency depression of the SOL H-reflex evoked by peroneal nerve stimulation (D2 inhibition) and an increase in the size of the monosynaptic Ia facilitation of the SOL H-reflex evoked by femoral nerve stimulation. These two measures provide independent evidence of changes in presynaptic inhibition of SOL Ia afferents and taken together suggest that GABAergic presynaptic inhibition of the SOL Ia afferents is decreased following 2 weeks of immobilization. The depression of the SOL H-reflex when evoked at intervals shorter than 10 s (homosynaptic post-activation depression) also decreased following immobilization, suggesting that the activity-dependent regulation of transmitter release from the afferents was also affected by immobilization. We observed no significant changes in disynaptic reciprocal Ia inhibition. Two weeks after cast removal measurements returned to pre-immobilization levels. Together, these observations suggest that disuse causes plastic changes in spinal interneuronal circuitries responsible for presynaptic control of sensory input to the spinal cord. This may be of significance for the motor disabilities seen following immobilization as well as the development of spasticity following central motor lesions.
机译:神经可塑性会随着成人的成熟,使用和废弃而发生。最近的研究表明,固定一段时间后,H反射幅度会增加。为了阐明导致固定后H反射大小增加的机制,我们在12名身体健康的受试者中固定了左脚和踝关节2周。在固定之前和之后以及恢复2周之后,测量比目鱼(SOL)运动神经元的突触倒数抑制和SOL组Ia传入神经的突触前控制。固定后,最大自主足底和背屈扭矩(MVC)显着降低,最大SOL H反射幅度增加,而最大复合运动反应(M(max))不变。 Ia传入神经突触前抑制的减少可能是H反射大小增加的原因,因为我们观察到腓神经刺激引起的SOL H反射长时程抑制显着降低(D2抑制),股神经刺激诱发的SOL H反射的单突触Ia大小。这两种措施提供了对SOL Ia传入神经突触前抑制作用变化的独立证据,两者合计表明,固定2周后,对GABA能的SOL Ia传入神经突触前抑制作用降低。固定后,短于10 s的间隔引起的SOL H反射的降低(突触后激活抑制)也降低了,这表明固定化也影响了传入递质释放的活性依赖性调节。我们没有观察到突触对等Ia抑制的显着变化。脱模后两周,测量值恢复到固定前的水平。在一起,这些观察结果表明,废用会导致负责突触控制脊髓感觉神经输入的脊髓神经元间回路的塑性变化。这对于固定后的运动障碍以及中枢性运动损伤后的痉挛发展可能具有重要意义。

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