Angelucci A, Clascá F, Sur M
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139, USA.
J Comp Neurol. 1998 Oct 26;400(3):417-39. doi: 10.1002/(sici)1096-9861(19981026)400:3<417::aid-cne10>3.0.co;2-o.
Following specific neonatal brain lesions in rodents and ferrets, retinal axons have been induced to innervate the medial geniculate nucleus (MGN). Previous studies have suggested that reduction of normal retinal targets along with deafferentation of the MGN are two concurrent factors required for the induction of novel retino-MGN projections. We have examined, in ferrets, the relative influence of these two factors on the extent of the novel retinal projection. We first characterized the inputs to the normal MGN, and the most effective combination of neonatal lesions to deafferent this nucleus, by injecting retrograde tracers into the MGN of normal and neonatally operated adult ferrets, respectively. In a second group of experiments, newborn ferrets received different combinations of lesions of normal retinal targets and MGN afferents. The resulting extent of retino-MGN projections was estimated for each case at adulthood, by using intraocular injections of anterograde tracers. We found that the extent of retino-MGN projections correlates well with the extent of MGN deafferentation, but not with extent of removal of normal retinal targets. Indeed, the presence of at least some normal retinal targets seems necessary for the formation of retino-MGN connections. The diameters of retino-MGN axons suggest that more than one type of retinal ganglion cells innervate the MGN under a lesion paradigm that spares the visual cortex and lateral geniculate nucleus. We also found that, after extensive deafferentation of MGN, other axonal systems in addition to retinal axons project ectopically to the MGN. These data are consistent with the idea that ectopic retino-MGN projections develop by sprouting of axon collaterals in response to signals arising from the deafferented nucleus, and that these axons compete with other sets of axons for terminal space in the MGN.
在啮齿动物和雪貂出现特定的新生儿脑损伤后，视网膜轴突已被诱导支配内侧膝状体（MGN）。先前的研究表明，正常视网膜靶标的减少以及MGN的传入神经切断是诱导新的视网膜 - MGN投射所需的两个同时存在的因素。我们在雪貂中研究了这两个因素对新的视网膜投射范围的相对影响。我们首先通过分别向正常和新生期接受手术的成年雪貂的MGN中注射逆行示踪剂，来表征正常MGN的输入以及使该核传入神经切断的最有效新生儿损伤组合。在第二组实验中，新生雪貂接受了正常视网膜靶标和MGN传入神经的不同损伤组合。成年后，通过眼内注射顺行示踪剂估计每种情况下视网膜 - MGN投射的范围。我们发现视网膜 - MGN投射的范围与MGN传入神经切断的程度密切相关，但与正常视网膜靶标去除的程度无关。实际上，至少存在一些正常视网膜靶标似乎是视网膜 - MGN连接形成所必需的。视网膜 - MGN轴突的直径表明，在一种使视觉皮层和外侧膝状体免受损伤的范式下，不止一种类型的视网膜神经节细胞支配MGN。我们还发现，在MGN广泛传入神经切断后，除了视网膜轴突外，其他轴突系统也异位投射到MGN。这些数据与以下观点一致：异位视网膜 - MGN投射是由轴突侧支响应去传入神经核产生的信号而萌发形成的，并且这些轴突与其他轴突组在MGN中竞争终末空间。
