Chiaia N L, Bennett-Clarke C A, Eck M, White F A, Crissman R S, Rhoades R W
Department of Anatomy, Medical College of Ohio, Toledo 43699.
J Neurosci. 1992 Jan;12(1):62-76. doi: 10.1523/JNEUROSCI.12-01-00062.1992.
Previous studies have shown that damage to vibrissa follicles in newborn rats and mice does not alter the brainstem representations of the remaining vibrissa as demonstrated by staining for mitochondrial enzymes such as cytochrome oxidase (CO) succinic dehydrogenase. This study asked whether this lack of effect might be due to the fact that the trigeminal primary afferents in rodents are already quite well developed at birth. We assessed this possibility by using CO staining the evaluate patterns in the brainstems of pre- and postnatal rats. A vibrissa-related pattern began to emerge in trigeminal nucleus principalis and subnucleus interpolaris (Spl) by embryonic day (E-) 19 and appeared fully developed by the day of birth (P-0). We also made partial lesions of the vibrissa pad on E-15-20 and on P-0, killed pups on P-5-7, and measured the size of the CO-stained patches in Spl on both sides of the brainstem. The correspondence between CO patches and clusters of primary afferent terminal arbors was verified in some animals by combining transganglionic horseradish peroxidase tracing and CO staining. Vibrissa pad damage on E-15-18 resulted in significant (20.1-36.9%) increases in the average area of the remaining CO patches in Spl ipsilateral to the lesion. Vibrissa pad damage on E-19, E-20, and P-0 produced small (6.2-8.9%), but insignificant, increases in patch size in Spl ipsilateral to the lesion. We used anatomical and electrophysiological methods to determine whether our lesions altered the trigeminal innervation of surviving vibrissa follicles. We recorded single trigeminal ganglion cells from 12 rats that sustained vibrissa pad lesion on E-17. As in normal rats, all of the 49 vibrissa-sensitive ganglion cells isolated in the lesioned animals were responsive to deflection of one and only one vibrissa. We also dissected 11 deep vibrissal nerves from intact follicles in adult rats that sustained fetal vibrissa pad damage on E-17, and counted numbers of myelinated axons in 1 microns plastic sections. These data were compared with counts from corresponding follicles on the intact side of the face. The average number of myelinated axons innervating follicles in the damaged vibrissa pads was 196.8 +/- 27.9, and that for the corresponding contralateral nerves was 194.6 +/- 25.7. These data suggest that competitive interactions among the central arbors of trigeminal primary afferents in fetal life may influence the development of central vibrissa representations and, further, that lesion-induced central changes need not be correlated with alterations in the peripheral innervation of undamaged follicles.
先前的研究表明，新生大鼠和小鼠的触须毛囊受损，并不会改变其余触须在脑干中的表征，这一点通过细胞色素氧化酶（CO）、琥珀酸脱氢酶等线粒体酶染色得以证明。本研究探讨了这种无影响的情况是否可能是由于啮齿动物的三叉神经初级传入纤维在出生时就已经相当发达。我们通过对产前和产后大鼠脑干进行CO染色来评估这种可能性。在胚胎第19天（E-19）时，与触须相关的模式开始在三叉神经主核和极间亚核（Spl）中出现，并在出生当天（P-0）完全发育成熟。我们还在E-15至E-20以及P-0时对触须垫进行部分损伤，在P-5至P-7时处死幼崽，并测量脑干两侧Spl中CO染色斑块的大小。在一些动物中，通过结合跨神经节辣根过氧化物酶追踪和CO染色，验证了CO斑块与初级传入终末树突簇之间的对应关系。E-15至E-18时触须垫损伤导致损伤同侧Spl中其余CO斑块的平均面积显著增加（20.1%-36.9%）。E-19、E-20和P-0时触须垫损伤导致损伤同侧Spl中斑块大小有小幅度增加（6.2%-8.9%），但不显著。我们使用解剖学和电生理学方法来确定我们的损伤是否改变了存活触须毛囊的三叉神经支配。我们从12只在E-17时遭受触须垫损伤的大鼠中记录单个三叉神经节细胞。与正常大鼠一样，在受损动物中分离出的49个对触须敏感的神经节细胞均只对一根且仅一根触须的偏转有反应。我们还从成年大鼠完整毛囊中解剖出11条深部触须神经，这些大鼠在胎儿期E-17时遭受触须垫损伤，并在1微米塑料切片中计数有髓轴突的数量。将这些数据与面部完整侧相应毛囊的计数进行比较。支配受损触须垫中毛囊的有髓轴突平均数量为196.8±27.9，而相应对侧神经的数量为194.6±25.7。这些数据表明，胎儿期三叉神经初级传入纤维中枢树突之间的竞争相互作用可能会影响中枢触须表征的发育，此外，损伤引起的中枢变化不一定与未受损毛囊的外周神经支配改变相关。
