DEPENDENCE OF DEVELOPING GROUP IA AFFERENTS ON NEUROTROPHIN-3
DEPENDENCE OF DEVELOPING GROUP IA AFFERENTS ON NEUROTROPHIN-3
复制标题
DOI：
10.1002/cne.903630211
复制
发表时间：
1995-12-11
影响因子：
2.5
通讯作者：
ERNFORS, P
中科院分区：
文献类型：
--
作者：
KUCERA, J;FAN, GP;ERNFORS, P
在出生时，Ia组本体感受传入和肌梭，其形成是Ia传入依赖性的，在携带神经营养素-3（NT-3 -/-）基因缺失的小鼠中不存在。通过光学和电子显微镜检查Ia传入纤维是否接触肌管，导致随后退化的纺锤体的形成，或者Ia传入纤维和纺锤体是否从未在胚胎天（E）10.5-18.5的NT-3 -/-小鼠中形成。三组数据表明，Ia神经元不发育，纺锤体不形成NT-S缺陷小鼠。首先，Ia传入神经的外周投射不支配NT-3 -/-小鼠的后肢，如肢体外周神经中神经纤维的缺乏和E13.5-E18.5时比目鱼肌中传入神经-肌肉接触和纺锤体的缺乏所反映的。第二，在NT-3不存在的情况下，Ia传入神经的中枢投射不支配脊髓，如在E13.5或E15.5时脊髓背根萎缩和从肢体肌肉组织到脊髓运动神经元的传入投射的缺乏所示。最后，在E10.5-E14.5的腰背根神经节（DRG），即在Ia传入神经支配脊髓和后肢之前或与之一致的发育阶段，突变小鼠比野生型小鼠小20-64%，这可能是因为在缺乏NT-3的胚胎中Ia神经元的胞体缺失。或存活，并且在缺乏NT-3的早期胎鼠中形成Ia传入投射提示NT-3可以通过在神经突向外生长到靶向神经支配区域之前操作的机制来调节神经元数目。因此，发育中的Ia神经元可能依赖于DRG固有的NT-3，然后才达到对来自骨骼肌或脊髓运动神经元的NT-3的潜在依赖性阶段。(C)1995 Wiley-Liss，Inc.
At birth, group Ia proprioceptive afferents and muscle spindles, whose formation is Ia afferent-dependent, are absent in mice carrying a deletion in the gene for neurotrophin-3 (NT-3 -/-). Whether Ia afferents contact myotubes, resulting in the formation of spindles which subsequently degenerate, or whether Ia afferents and spindles never form was examined in NT-3 -/- mice at embryonic days (E) 10.5-18.5 by light and electron microscopy. Three sets of data indicate that Ia neurons do not develop and spindles do not form in NT-S-deficient mice. First, peripheral projections of Ia afferents did not innervate hindlimbs of NT-3 -/- mice, as reflected by a deficiency of nerve fibers in limb peripheral nerves and an absence of afferent nerve-muscle contacts and spindles in the soleus muscle at E13.5-E18.5. Second, central projections of Ia afferents did not innervate the spinal cord in the absence of NT-3, as shown by an atrophy of the dorsal spinal roots and absence of afferent projections from limb musculature to spinal motor neurons at E13.5 or E15.5. Lastly, the lumbar dorsal root ganglia (DRGs) at E10.5-E14.5, the stages of development that precede or coincide with the innervation of the spinal cord and hindlimbs by Ia afferents, were 20-64% smaller in mutant than in wild-type mice, presumably because the cell bodies of Ia neurons were absent in embryos lacking NT-3.The failure of Ia neurons to differentiate and/or survive and Ia afferent projections to form in early fetal mice lacking NT-3 suggests that NT-3 may regulate neuronal numbers by mechanisms operating prior to neurite outgrowth to target innervation fields. Thus, developing Ia neurons may be dependent on NT-3 intrinsic to the DRGs before they reach a stage of potential dependence on NT-3 retrogradely derived from skeletal muscles or spinal motor neurons. (C) 1995 Wiley-Liss, Inc.