Plasticity of synaptic endings in the cochlear nucleus following noise-induced hearing loss is facilitated in the adult FGF2 overexpressor mouse


Dr D. Kent Morest, as above.


In adult mammals a single exposure to loud noise can damage cochlear hair cells and initiate subsequent episodes of degeneration of axonal endings in the cochlear nucleus (CN). Possible mechanisms are loss of trophic support and/or excitotoxicity. Fibroblast growth factor 2 (FGF2), important for development, might be involved in either mechanism. To test this hypothesis, we noise-exposed FGF2 overexpressor mice and observed the effects on synaptic endings by immunolabelling for SV2, a synaptic vesicle protein, at 1, 2, 4, and 8 weeks after noise exposure. SV2 staining was observed in two major locations; perisomatic, representing axo-somatic terminals, and neuropil, representing axo-dendritic terminals. The wildtype (WT) lost both perisomatic and neuropil clusters with an intervening period of modest recovery for the perisomatic. In contrast, in the overexpressor, the perisomatic clusters remained unchanged after intervening periods of increase. The neuropil clusters underwent a period of initial decline, followed by a transient recovery and ultimate decline. Changes in SV2 immunostaining correlated with changes in vesicular glutamate and GABA transporters at synapses and, in the overexpressor, with staining changes for FGF2 and FGF receptor 1. These molecules may contribute to the synaptic reorganization after noise damage; they may protect and/or aid recovery of synapses after overstimulation.