Personius K E., Chapman R F.
Interdisciplinary Program in Physiological Sciences Graduate Program and ARL Division of Neurobiology, University of Arizona, 85721, Tucson, AZ, USA
J Insect Physiol. 2002 Jan;48(1):91-102. doi: 10.1016/s0022-1910(01)00149-4.
When the grasshopper, Barrytettix humphreysii, sheds a hindlimb during autotomy, certain thoracic muscles degenerate although they are neither directly damaged nor denervated. Muscle degeneration is induced when a leg nerve (N5) that does not innervate the thoracic muscles is severed. Together these results suggest that transneuronal mechanisms influence muscle survival. To further characterize this autotomy-induced process, we studied the degeneration of a thoracic tergotrochanteral muscle (M#133b,c) following autotomy or experimental manipulation in adult animals. Its degeneration is correlated with reduced activity of its neural input and occurs by programmed cell death (PCD). PCD onset is variable between individual muscle fibers, indicating that the trigger of degeneration is fiber specific. Muscle degeneration appears to be triggered by the loss of proprioceptive input from the autotomized limb, since severing of axons from proprioceptive organs, but not exteroceptive chemo- or mechanoreceptors, leads to muscle degeneration. Muscle disuse, neuronal degeneration, or changes in juvenile hormone titer do not appear to play a role in autotomy-induced degeneration. We propose that the loss of proprioceptive input from proximal campaniform sensilla on the tibia deafferents the thoracic muscle motor neurons and leads to a decrease in their activity. Muscle degeneration is ultimately triggered by the loss of normal neural activity.
当蚱蜢(Barrytettix humphreysii)在自切过程中脱落一条后肢时,某些胸部肌肉会退化,尽管它们既没有直接受损也没有去神经支配。当一条不支配胸部肌肉的腿部神经(N5)被切断时,肌肉退化就会被诱导。这些结果共同表明跨神经元机制会影响肌肉存活。为了进一步表征这种自切诱导的过程,我们研究了成年动物自切或实验操作后胸部的一块背转子肌(M#133b、c)的退化情况。它的退化与其神经输入活动的降低相关,并通过程序性细胞死亡(PCD)发生。PCD的起始在单个肌纤维之间是可变的,这表明退化的触发是纤维特异性的。肌肉退化似乎是由自切肢体本体感觉输入的丧失触发的,因为切断本体感觉器官的轴突会导致肌肉退化,而切断外感受性化学或机械感受器的轴突则不会。肌肉废用、神经元退化或保幼激素滴度的变化似乎在自切诱导的退化中不起作用。我们提出,来自胫节近端钟形感受器的本体感觉输入的丧失使胸部肌肉运动神经元去传入,并导致其活动减少。肌肉退化最终是由正常神经活动的丧失触发的。