Plasticity of the auditory brainstem: effects of cochlear ablation on GAP-43 immunoreactivity in the rat.

Abstract

In the adult brain, expression of the growth associated protein GAP-43 may serve as an indicator of synaptic remodeling. We have studied localization and time course of the re-expression of GAP-43 following deafening through cochlear ablation. As a consequence of unilateral cochlear lesioning, a substantial increase in the expression of GAP-43 was observed in the neuropil of all subnuclei of the ipsilateral cochlear nuclear complex. This expression of GAP-43 occurred in well-defined fibers and boutons. In the ventral cochlear nuclei, boutons immunoreactive for GAP-43 were often localized on cell bodies. However, they were found only on selected subpopulations of cochlear nucleus neurons, i.e., on cell bodies containing glutamate or calretinin immunoreactivity, but apparently not on GABAergic neurons. Olivocochlear neurons must have been axotomized by the operation. Following cochlear ablation, a dramatic re-expression of GAP-43 occurred in cell bodies of the ipsilateral lateral superior olive but not in the ventral nucleus of the trapezoid body. Position and number of these cells suggested that most, if not all, of them serve the lateral olivocochlear bundle. However, although axon collaterals are given off by certain types of olivocochlear neurons, a direct involvement of the immunoreactive cell bodies in the emergence of GAP-43 in the cochlear nucleus is not obvious. A transient rise of GAP-43 immunoreactivity that could not be attributed to axotomized neurons was observed in the contralateral dorsal cochlear nucleus and in the ipsilateral inferior colliculus. Given the functional significance attributed to GAP-43, we conclude that the sudden loss of spiral ganglion cells leads to a reactive synaptogenesis in complex patterns across several auditory brainstem nuclei.