title: Lesion-induced establishment of the crossed corticorubral projections in kittens is associated with axonal proliferation and topographic refinement.
abstract: The aberrant crossed corticorubral projection of the cat, which is very weak compared to the uncrossed one at about 1 month postnatal, becomes pronounced following unilateral lesions of the sensorimotor cortex. In order to determine whether or not terminal proliferation of pre-existing axons underlie this enlargement, the morphological changes of the crossed axons were examined, using the anterograde tracer Phaseolus vulgar- is leukoagglutinin (PHA-L). The crossed corticorubral axons in normal kittens were mostly simple in morphology with infrequent branching and did not often exhibit growth-cone-like axonal endings at 1 month postnatal. Two to 5 days after unilateral lesions of the sensorimotor cortex placed at this age, the axons were as simple as those in normal animals but ended in growth cones more frequently. Seven to 10 days post-lesion, the axons often bore side-branches which ended in growth cones. Two to 3 weeks post-lesion axons with sprays of finger-like fine sprouts occurred throughout the projection zone. There was no clear topography for the crossed projection in normal animals, but at 1-2 weeks post-lesion the axons started to show a certain amount of localization in the regions of the red nucleus which corresponded to the densely innervated region on the ipsilateral side. The topography of the crossed projections roughly mirrors that of the ipsilateral projection at about 1 month post-lesion. Thus, the lesions of the sensorimotor cortex induce substantial growth and proliferation of the crossed corticorubral axons. The post-lesion changes in axonal morphology and topographic refinement are reminiscent of developmental events. It is likely that the lesions permit the crossed axons, which normally fail to develop, to develop like the uncrossed ones.
authors.affiliation: Department of Biophysical Engineering, Faculty of Engineering Science, Osaka University, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Murakami
authors.forename: S
authors.initials: S
authors.lastname: Higashi
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: A
authors.initials: A
authors.lastname: Tamada
mesh_terms: D000375:Aging; D000818:Animals; D001370:Axonal Transport; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D001921:Brain / Q000254:growth & development / Q000502:physiology*; D002415:Cats; D002540:Cerebral Cortex / Q000502:physiology*; D007839:Functional Laterality; D009473:Neuronal Plasticity; D010835:Phytohemagglutinins; D012012:Red Nucleus / Q000166:cytology / Q000502:physiology*
chemical_list: D010835:Phytohemagglutinins; C100156:leukoagglutinins, plants