Castro-Moure F, Goshgarian H G
Department of Anatomy and Cell Biology, Wayne State University, School of Medicine, Detroit, Michigan 48201, USA.
Exp Neurol. 1997 Oct;147(2):299-310. doi: 10.1006/exnr.1997.6615.
Morphological plasticity occurs in the phrenic nucleus within hours following an ipsilateral C2 spinal cord hemisection. The plasticity has been associated with the unmasking of a latent respiratory pathway (the crossed phrenic pathway) which allows recovery of the hemidiaphragm paralyzed by the hemisection during a reflex known as the crossed phrenic phenomenon. This study tests if the plasticity is induced by the generalized effects of spinal cord trauma or the more specific effect of interrupting the main descending respiratory drive to phrenic motoneurons. Electron microscopic quantitative morphometric analysis of the phrenic nucleus neuropil was carried out on four Sprague-Dawley rats (200-250 g) sacrificed 4 h following unilateral reversible cold block of the descending bulbospinal respiratory drive at the second cervical segment of the spinal cord (C2). The data from four sham-operated control animals were compared with those of the experimental group. The following morphological alterations were documented in cold block animals compared to controls: (1) a significant increase in the number of multiple synapses (i.e., terminals with synaptic active zones contacting two or more postsynaptic profiles in the same plane of section), (2) a significant increase in the number of dendrodendritic appositions, and (3) a significant increase in the length of symmetric and asymmetric synaptic active zones. The above changes are similar to the changes induced in the phrenic nucleus following C2 hemisection. We conclude therefore, that injury to the spinal cord is not a requirement for this type of morphological plasticity in the phrenic nucleus, but rather the induced changes are activity-dependent and are likely caused by the interruption of the descending bulbospinal respiratory drive to the phrenic nucleus.
在同侧C2脊髓半横断后数小时内,膈神经核会出现形态可塑性。这种可塑性与一条潜在呼吸通路(交叉膈神经通路)的显露有关,该通路能使在一种称为交叉膈神经现象的反射过程中因半横断而麻痹的半侧膈肌恢复功能。本研究旨在测试这种可塑性是由脊髓损伤的全身性影响引起,还是由中断膈运动神经元的主要下行呼吸驱动这一更具体的影响所致。对4只体重200 - 250克的Sprague-Dawley大鼠进行了膈神经核神经毡的电子显微镜定量形态计量分析,这些大鼠在脊髓第二颈段(C2)对下行延髓脊髓呼吸驱动进行单侧可逆性冷阻断4小时后被处死。将4只假手术对照动物的数据与实验组的数据进行比较。与对照组相比,冷阻断动物出现了以下形态学改变:(1)多个突触(即突触活性区的终末在同一截面平面内与两个或更多突触后轮廓接触)的数量显著增加;(2)树-树并置的数量显著增加;(3)对称和不对称突触活性区的长度显著增加。上述变化与C2半横断后膈神经核所诱导的变化相似。因此,我们得出结论,脊髓损伤并非膈神经核这种类型形态可塑性的必要条件,相反,所诱导的变化是活动依赖性的,很可能是由下行延髓脊髓呼吸驱动对膈神经核的中断所致。