Elsevier

Experimental Neurology

Volume 30, Issue 2, February 1971, Pages 336-351
Experimental Neurology

Axonal regeneration and formation of synapses proximal to the site of lesion following hemisection of the rat spinal cord

https://doi.org/10.1016/S0014-4886(71)80012-2Get rights and content

Although the central nervous system of the mammal is reported not to regenerate, axonal sprouting has recently been demonstrated in various regions of brain and spinal cord. The following study investigates the regenerative capacity of 72 rat spinal cords following left hemisection at T2. In addition to nine normals, rats were killed at 5, 7, 14, 30, 60, and 90 days after making the lesion. Three animals per groups were prepared for Golgi, Protargol-eosin-cresyl violet staining, and electron microscopy. Three additional animals had hemisections at C5 and the cord from C5 to T5 was stained by the Fink-Heimer method. Six animals had hemisections at T2 and the cords were subsequently rehemisected 90 days later at C5; three animals were prepared for the Fink-Heimer stain and three for electron microscopy. The dendrites of the reactive motor neurons proximal to the site of lesion became varicose from day 10 to day 60–90 after the lesion, until the entire dendrite was replete with irregularly shaped varicosities. At 15 days postoperatively, processes grew into the reactive neural zone and by day 30 could be identifified as axons (0.1–0.5 μ in diameter) and dendrites. The axons grew in fascicles, usually free of neuroglial cell processes. The amjority of the axons formed axodendritic synapses on the indentations of the dendritic varicosities by 60–90 days postoperatively. The Fink-Heimer stain reveled that a limited number of axons regenerated from long tracts into the reactive neural zone. Most regenerated axons appear to be axonal sprouts from the operated and unoporated portions of the spinal cord. The central nervous system of the rat does regenerate, but the regenerating axons do not grow past the reactive neural zone and thus do not reach the neuroglial scar.

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    Supported by NIH grant NS 06164 (HEW).

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