Dendrite-derived supernumerary axons on adult axotomized motor neurons possess proteins that are essential for the initiation and propagation of action potentials and synaptic vesicle release

Axotomy can trigger profound alterations in the neuronal polarity of adult neurons in vivo. This can manifest itself in the development of new axon-like processes emanating from the tips of distal dendrites. Previously, these processes have been defined as axonal based on their axonal morphology. Th...

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Published inThe Journal of neuroscience Vol. 31; no. 18; pp. 6732 - 6740
Main Authors Meehan, Claire F, MacDermid, Victoria E, Montague, Steven J, Neuber-Hess, Monica, Rose, P Ken
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 04.05.2011
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Summary:Axotomy can trigger profound alterations in the neuronal polarity of adult neurons in vivo. This can manifest itself in the development of new axon-like processes emanating from the tips of distal dendrites. Previously, these processes have been defined as axonal based on their axonal morphology. This study extends this definition to determine whether, more importantly, these processes possess the prerequisite molecular machinery to function as axons. Using a combination of intracellular labeling and immunohistochemistry, we demonstrate that the distribution of voltage-gated sodium channels on these processes matches the arrangement of these channels that is necessary for the initiation and conduction of action potentials. At terminal bouton-like structures they possess key proteins necessary for the release of synaptic vesicles (SV2 and synaptophysin). Thus, axon-like processes emanating from the tips of distal dendrites represent a rearrangement of neuronal polarity whereby axotomized neurons can develop additional functional axons in vivo.
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Author contributions: C.F.M. and P.K.R. designed research; C.F.M., V.E.M., S.J.M., M.N.-H., and P.K.R. performed research; C.F.M., V.E.M., and M.N.-H. analyzed data; C.F.M. and P.K.R. wrote the paper.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.5377-10.2011