Anatomy, development and lesion-induced plasticity of rodent corticospinal tract.
In this review the current knowledge of the anatomy, development and plasticity of the rodent corticospinal tract is summarised. Recent technical advancements, especially in neuronal tracing methods, have provided much new data concerning the anatomy of the corticospinal tract. The rodent corticospinal axons project to the subcortical nuclei via collateral branches. These collateral branches of corticospinal axons are formed by delayed interstitial budding during early postnatal periods. Corticospinal neurons are generated in the ventricular zone during a short time lag, migrate into the cortical plate, and settle in layer V of the cerebral cortex. The migration of corticospinal neurons is experimentally deranged by prenatal exposure to alcohol or genetically affected by the reeler genetic locus (rl), resulting in generation of ectopic corticospinal neurons. Such experimentally or genetically induced ectopic corticospinal neurons are a good model for examining whether target recognition and path finding are affected by the intracortical position of corticospinal neurons. Some chemical molecules (e.g. L1 and B-50/GAP43) are transiently expressed in the corticospinal tract during the perinatal period, while others (e.g. protein kinase C gamma subspecies and alpha CaM kinase II) are permanently expressed in the adult corticospinal tract. The only chemical marker specific for layer V corticofugal neurons is an antibody to a soluble protein, protein 35. Since the corticospinal tract in the rodent is an easily identified group of fibers situated in the most ventral portion of the dorsal funiculus of the spinal cord and exhibits considerable postnatal development, it has often been utilized in the neurological studies on plasticity and regenerative capacity of the lesioned central nervous system. Recently, it has been clarified that growing corticospinal fibers have the ability to penetrate and traverse across the lesion sites under certain special conditions.
Terashima
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Department of Anatomy, Tokyo Metropolitan Institute for Neuroscience, Japan.
D000818:Animals; D051379:Mice; D009473:Neuronal Plasticity / Q000502:physiology*; D011712:Pyramidal Tracts / Q000033:anatomy & histology* / Q000166:cytology / Q000196:embryology; D051381:Rats; D012377:Rodentia / Q000033:anatomy & histology* / Q000196:embryology