Lack of growth-associated protein-43 reemergence or of growth-associated protein-43 mRNA modulation in deafferented vestibular nuclei during the first 6 weeks after unilateral inner ear lesion

We investigated whether a unilateral inner ear lesion that destroyed the la byrinthine receptors, the cochlear receptors, and the spiral ganglion induc ed callateral sprouting in rat vestibular and auditory brainstem nuclei, us ing growth-associated protein-43 (GAP-43) as an indicator of synaptic remod eling. Both immunocytochemistry and in situ hybridization were performed to detect a potential modulation of GAP-43 and of its messenger RNA (mRNA) at different times after surgery. We failed to observe a reemergence of GAP-4 3 or a modulation of its mRNA in the deafferented vestibular nuclei at all survival times tested. In contrast, a substantial increase in the expressio n of GAP-43 was observed in the neuropil of the ipsilateral deafferented co chlear nuclei and in cell bodies of the ipsilateral superior olive. This in crease was associated with an up- and downregulation of the mRNA coding for GAP-43 in the ipsilateral ventral cochlear nucleus and in the ipsilateral superior olive, respectively. These data indicate that synaptic remodeling, as assessed by GAP-43 expression, does not seem to occur in the deafferent ed vestibular complex during the first 6 weeks after labyrinthectomy, where as it occurs within the first deafferented auditory relays at times as earl y as 4 days following spiral ganglion and cochlear receptors removal. We co nclude that recovery of a normal resting discharge of the deafferented cent ral vestibular neurons and consequently recovery of a normal resting postur e and eye position may not depend on collateral sprouting of the remaining vestibular afferents. In contrast, we confirmed that a reactive synaptogene sis occurs in the brainstem auditory nuclei following cochlea and spiral ga nglion removal. Its functional significance remains an open question.