Denervation of non‐optic brain areas along the course of the optic tract does not affect the success of optic nerve regeneration in frogs

Abstract

AbstractUnsuccessful axonal regeneration in frog or goldfish spinal cord is thought to be due in part to inappropriate denervated synaptic sites attracting regenerating axons as they pass by the lesion zone (Bernstein and Bernstein, '69; Bernstein and Gelderd, '73). The reported success of optic nerve regeneration in these same animals may result because there are no inappropriate synaptic sites available to the regenerating axons. To test for this we denervated areas within thalamus and mesencephalon which lie along the path of regenerating optic axons to determine whether or not abnormal connections would form in these areas and affect the success of optic nerve regeneration. After transection of the brainstem through the isthmal region, terminal degeneration was found in several zones adjacent to optic nerve targets or the optic tract (i.e., nucleus rotundus, corpus geniculatum laterale, and torus semicircularis). In adult frogs receiving left isthmal transection, we also crushed the right optic nerve and then examined the regenerated optic projection at intervals up to six months after nerve crush using anterograde transport of 3H‐proline. In no instance did the regenerating optic axons alter their distribution within visual neuropil zones or invade those areas deafferented by the isthmal lesion. Histological study showed that the axons cut by the isthmal lesion did not regenerate back to their sites to prevent the invasion of optic axons into these zones. We then attempted to force optic axons into foreign territory by removing a major projection zone, the optic tectum. With tectal ablation and isthmal transection, regenerating optic axons were offered synaptic space made available by both lesions. However, we found abnormal optic projections only in the middle and posterior thalamic neuropil and in the remaining tectal hemisphere. Optic axons did not expand into any of the areas deafferented by the isthmal transection, even though some of them were further denervated by the tectal ablation. We conclude that optic axons will not invade non‐optic areas deafferented by an isthmal lesion even if a large number of optic axons have no normal target to innervate.