The effect of axon injury on microtubule-associated proteins MAP2, 3 and 5 in the hypoglossal nucleus of the adult rat

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Abstract
Microtubule-associated proteins appear to be critical elements in the stabilization of microtubules during neurite development. Axon injury results in a new burst of axonal growth activity as well as in partial dendritic involution. With this background we have examined the immunocytochemical staining pattern for microtubule-associated proteins 2,3 and 5 in the hypoglossal nucleus of adult rats following unilateral hypoglossal nerve resection. From four days to six weeks postlesion a significant reduction in microtubule-associated protein 2-like immunoreactivity was observed in the neuropil and neuronal perikarya of the hypoglossal nucleus ipsilateral to nerve transaction. Microtubule-associated protein 5-like immunoreactivity was reduced in neuronal perikarya and neuropil four days to two weeks after injury. After six weeks microtubule-associated protein 5-like immunoreactivity had returned to normal levels. Microtubule-associated protein 3-like immunoreactivity, which was observed in glial cell perikarya and axons, but not neuronal perikarya or dendrites, appeared to be essentially unaltered. The reduced levels of microtubule-associated proteins 2 and 5 may be factors contributing to previously documented axotomy-induced dendritic retraction. The decrease in microtubule-associated protein 5 staining and absence of microtubule-associated protein 3 expression in axotomized neurons contrast with the situation in developing neurons, and demonstrate that the neuronal reaction to axon injury in mature mammals involves a specific series of events distinct from the developmental process.

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