Morphological alteration of thalamic afferents in the excitotoxically lesioned striatum.

Excitotoxic lesions of the neostriatum cause anatomical and biochemical changes resembling those occurring in Huntington's disease. One major characteristic of these lesions is that they acutely spare axons of passage and afferent fibers. However, evidence is accumulating that afferent axonal systems decrease their fiber density in the long-term excitotoxic lesion. Ultrastructural changes of neuron-deprived terminals may also occur. A parallel study considering changes in afferent fibers to the excitotoxically lesioned thalamus showed that, a few weeks after neuron-depletion, specific 'point-to-point' systems formed regenerating axonal growth cone-like structures. The present study used the anterograde transport of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to determine whether specific thalamostriatal afferents form the same kind of regenerating structures following excitotoxic lesion of their target neurons. Thalamostriatal afferents decreased in density over months after lesion, but some were still labeled as long as 4 months after ibotenic acid injection. Remaining afferents formed axonal growth cone-like structures, identified at both light and electron microscopic levels, similar to those observed in the lesioned thalamus. These results demonstrate that in the striatum as in the thalamus, neuron depletion is followed by a long-term alteration of the morphology of some afferent fibers which form regenerating growth cone-like structures. These results are discussed with regard to the possible functional integration of fetal neurons transplanted into previously excitotoxically lesioned areas.