Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Prog Brain Res. 2011;188:167-80. doi: 10.1016/B978-0-444-53825-3.00016-4.
We established that hyperreflexia is delayed after spinal transection in the adult rat and that passive exercise could normalize low frequency-dependent depression of the H-reflex. We were also able to show that such passive exercise will normalize hyperreflexia in patients with spinal cord injury (SCI). Recent results demonstrate that spinal transection results in changes in the neuronal gap junction protein connexin 36 below the level of the lesion. Moreover, a drug known to increase electrical coupling was found to normalize hyperreflexia in the absence of passive exercise, suggesting that changes in electrical coupling may be involved in hyperreflexia. We also present results showing that a measure of spasticity, the stretch reflex, is rendered abnormal by transection and normalized by the same drug. These data suggest that electrical coupling may be dysregulated in SCI, leading to some of the symptoms observed. A novel therapy for hyperreflexia and spasticity may require modulation of electrical coupling.
我们已经确定，在成年大鼠的脊髓横切后，反射亢进会延迟，而被动运动可以使低频依赖的 H 反射抑制正常化。我们还能够证明，这种被动运动可以使脊髓损伤（SCI）患者的反射亢进正常化。最近的研究结果表明，脊髓横切导致损伤以下神经元间隙连接蛋白连接蛋白 36 的变化。此外，发现一种已知可增加电耦合的药物可在没有被动运动的情况下使反射亢进正常化，这表明电耦合的变化可能与反射亢进有关。我们还提供了一些结果，表明一种痉挛测量指标，即牵张反射，在横切后变得异常，并通过相同的药物正常化。这些数据表明，电耦合可能在 SCI 中失调，导致观察到的一些症状。治疗反射亢进和痉挛的新疗法可能需要调节电耦合。
