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Cochlear damage induces GAP‐43 expression in cholinergic synapses of the cochlear nucleus in the adult rat: a light and electron microscopic study
Author(s) -
Meidinger Markus A.,
HildebrandtSchoenfeld Heika,
Illing RobertBenjamin
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04853.x
Subject(s) - cochlear nucleus , cholinergic , nucleus , choline acetyltransferase , biology , synaptic vesicle , ultrastructure , gap junction , neuroscience , vesicle , gap 43 protein , brainstem , synaptic plasticity , anatomy , microbiology and biotechnology , immunohistochemistry , membrane , biochemistry , receptor , immunology , intracellular
Recent studies suggest a potential for activity‐dependent reconstruction in the adult mammalian brainstem that exceeds previous expectations. We found that a unilateral cochlear lesion led within 1 week to a rise of choline acetyltransferase (ChAT) immunoreactivity in the ventral cochlear nucleus of the affected side, matching the lesion‐induced expression of growth‐associated protein 43 (GAP‐43) previously described. The rise of both ChAT and GAP‐43 immunoreactivity was reflected in the average density of the staining. Moreover, the number of light‐microscopically identifiable boutons increased in both stains. GAP‐43‐positive boutons could, by distinct ultrastructural features, regularly be identified as presynaptic endings. However, GAP‐43 immunoreactivity was not only found in presynaptic endings with a classical morphology, but also in profiles that suggest morphological dynamic structures by showing filopodia, assemblages of pleomorphic vesicles, large vesicles (diameter up to 200 nm) fusing with the presynaptic plasma membrane close to synaptic contacts, small dense‐core vesicles (diameter about 80 nm) and presynaptic ribosomes. Moreover, we observed perforated synapses as well as GAP‐43 immunoreactivity condensed in rafts, both indicative of growing or changing neuronal connections. Classical and untypical ultrastructural profiles that contained GAP‐43 also contained ChAT. We conclude that there is extensive deafness‐induced GAP‐43‐mediated synaptic plasticity in the cochlear nucleus, and that this plasticity is predominantly, if not exclusively, based on cholinergic afferents.