Sotelo C
INSERM U 106, Hôpital de la Salpétrière, 47 bd de l'Hôpital, Paris.
J Physiol (Paris). 1991;85(3):134-44.
Neurological mutations affecting the cerebellum of the mouse have offered the possibility to study some of the cellular mechanisms involved in the establishment of synaptic connections (see in Sotelo, 1990). Indeed, these mutations provoke through well-defined lesions, the disruption of the normal processes of synapse formation and, by examination of the perturbations in the adult cerebellar connectivity, it is possible to unravel some of the numerous and intricate cellular interactions taking place during synaptogenesis. Furthermore, some of these mutants primarily affect Purkinje cells, the pivotal elements of the cerebellar cortex and its only output, inducing their degeneration. These Purkinje cell-deficient cerebella offer an optimal material to try--by grafting experiments--to replace the missing neurons, and to analyze synaptogenic processes between neuronal partners of different biological ages: the host adult neurons and the embryonary grafted Purkinje cells (Sotelo et al., 1990). The aim of this paper is to summarize some of the work carried out in my laboratory concerning the two above-mentioned topics.
影响小鼠小脑的神经学突变提供了研究一些参与突触连接建立的细胞机制的可能性（见索特洛，1990年）。确实，这些突变通过明确的损伤引发突触形成正常过程的破坏，并且通过检查成年小脑连接性的扰动，有可能揭示在突触发生期间发生的众多复杂细胞相互作用中的一些。此外，其中一些突变主要影响浦肯野细胞，即小脑皮质的关键元素及其唯一输出，导致它们退化。这些缺乏浦肯野细胞的小脑提供了一种理想的材料，通过移植实验来尝试替代缺失的神经元，并分析不同生物学年龄的神经元伙伴之间的突触发生过程：宿主成年神经元和胚胎移植的浦肯野细胞（索特洛等人，1990年）。本文的目的是总结在我的实验室中关于上述两个主题所开展的一些工作。
