Emergence of axons from distal dendrites of adult mammalian neurons following a permanent axotomy

Citation
Pk. Rose et al., Emergence of axons from distal dendrites of adult mammalian neurons following a permanent axotomy, EUR J NEURO, 13(6), 2001, pp. 1166-1176
Citations number
37
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EUROPEAN JOURNAL OF NEUROSCIENCE
ISSN journal
0953816X → ACNP
Volume
13
Issue
6
Year of publication
2001
Pages
1166 - 1176
Database
ISI
SICI code
0953-816X(200103)13:6<1166:EOAFDD>2.0.ZU;2-V
Abstract
The distinctive features of axons and dendrites divide most neurons into tw o compartments. This polarity is fundamental to the ability of most neurons to integrate synaptic signals and transmit action potentials. It is not kn own, however, if the polarity of neurons in the adult mammalian nervous sys tem is fixed or plastic. Following axotomy, some distal dendrites of neck m otoneurons in the adult cat give rise to unusual processes that, at a light microscopic level, resemble axons (Rose, P.K. & Odlozinski, M., J. Comp. N eurol., 1998, 390, 392). The goal of the present experiments was to charact erize these unusual processes using well-established ultrastructural and mo lecular criteria that differentiate dendrites and axons. These processes we re immunoreactive for growth-associated protein-43 (GAP-43), a protein that is normally confined to axons. In contrast, immunoreactivity for a protein that is widely used as a marker for dendrites, microtubule-associated prot ein (MAP)-2a/b, could not be detected in the unusual distal arborizations. At the electron microscopic level, unusual distal processes contained dense collections of neurofilaments and were frequently myelinated. These molecu lar and structural characteristics are typical of axons and suggest that th e polarity of adult neurons in the mammalian nervous system can be disrupte d by axotomy. If this transformation in neuronal polarity is common to othe r types of neurons, axon-like processes emerging from distal dendrites may represent a mechanism for replacing connections lost due to injury. Alterna tively, the connections formed by these axons may be aberrant and therefore maladaptive.