Fike E A, Simons E, Boswell C, Smith P G
Department of Physiology, University of Kansas Medical Center, Kansas City 66160-7401.
Exp Neurol. 1992 Oct;118(1):85-94. doi: 10.1016/0014-4886(92)90025-l.
Neuronal populations projecting to a common target may compete for neurotrophic substances. To determine if competition impairs target reinnervation, we examined the effect of capsaicin-induced sensory denervation on sympathetic nerve ingrowth to the sympathectomized rat superior tarsal smooth muscle. In tarsal muscles with intact sympathetic innervation, capsaicin injection on Day 2 reduced numbers of perimuscular CGRP-ir sensory nerves by 68% at 3-4 months; however, it did not alter dopamine-beta-hydroxylase-ir nerve density, response to nerve stimulation, or tarsal muscle adrenoceptor-mediated contraction. Tarsal muscles denervated by ipsilateral superior cervical ganglionectomy on Postnatal Day 4 were partially reinnervated by fibers from the contralateral ganglion, as noted in previous studies. Sensory denervation by capsaicin improved sympathetic reinnervation, as evidenced by a 174% increase in numbers of DBH-ir nerves and a 62% increase in neurally mediated smooth muscle contraction evoked by electrical stimulation of the contralateral pathway relative to reinnervated muscles of vehicle-injected rats; smooth muscle function was also influenced, as indicated by a decrease toward normal in adrenoceptor sensitivity. Tarsal muscles denervated at 30 days were not reinnervated in either vehicle-injected or capsaicin-treated rats, indicating that sensory denervation does not extend the developmental window during which contralateral reinnervation can occur. Both the vehicle-injected and capsaicin-treated preparations with sustained juvenile sympathectomy showed sensory hyperinnervation as adults; thus, a chronic reduction in competition from sympathetics is a sufficiently powerful stimulus to overcome the decreased nerve density induced by neonatal capsaicin treatment. We conclude that sensory nerves limit the extent of sympathetic reinnervation and functional recovery that can occur following neonatal sympathetic denervation.
投射至共同靶标的神经元群体可能会竞争神经营养物质。为了确定竞争是否会损害靶标再支配，我们研究了辣椒素诱导的感觉去神经对交感神经长入去交感神经支配的大鼠上睑提肌平滑肌的影响。在交感神经支配完整的睑肌中，第2天注射辣椒素可使3 - 4个月时肌周降钙素基因相关肽免疫反应性（CGRP-ir）感觉神经数量减少68%；然而，它并未改变多巴胺-β-羟化酶免疫反应性（dopamine-beta-hydroxylase-ir）神经密度、对神经刺激的反应或睑肌肾上腺素能受体介导的收缩。如先前研究所述，出生后第4天经同侧颈上神经节切除术去神经支配的睑肌，会被来自对侧神经节的纤维部分再支配。辣椒素诱导的感觉去神经改善了交感神经再支配，相对于注射赋形剂大鼠的再支配肌肉，经对侧通路电刺激诱发的多巴胺-β-羟化酶免疫反应性（DBH-ir）神经数量增加174%，神经介导的平滑肌收缩增加62%，这证明了这一点；肾上腺素能受体敏感性向正常水平降低也表明平滑肌功能受到了影响。在30天时去神经支配的睑肌，在注射赋形剂或辣椒素处理的大鼠中均未实现再支配，这表明感觉去神经并不会延长对侧再支配可能发生的发育窗口期。持续进行幼年交感神经切除术的注射赋形剂和辣椒素处理的标本在成年后均表现出感觉神经纤维过度生长；因此，来自交感神经的竞争长期减少是一个足够强大的刺激，能够克服新生期辣椒素处理诱导的神经密度降低。我们得出结论，感觉神经限制了新生期交感神经去神经支配后可能发生的交感神经再支配和功能恢复的程度。
