The impact of neurotrophin-3 on the dorsal root transitional zone following injury.
METHODS
Morphological and Stereological assessment of the dorsal root transitional zone (DRTZ) following complete crush injury, using light microscopy (LM) and transmission electron microscopy (TEM).


OBJECTIVE
To assess the effect of exogenous neurotrophin-3 (NT-3) on the response of glial cells and axons to dorsal root damage.


METHODS
Department of Anatomy, University College Cork, Ireland and Department of Physiology, UMDS, University of London, UK.


METHODS
Cervical roots (C6-8) from rats which had undergone dorsal root crush axotomy 1 week earlier, in the presence (n=3) and absence (n=3) of NT-3, were processed for LM and TEM.


RESULTS
Unmyelinated axon number and size was greater in the DRTZ proximal (Central Nervous System; CNS) and distal (Peripheral Nervous System; PNS) compartments of NT-3-treated tissue. NT-3 was associated with a reduced astrocytic response, an increase in the proportion of oligodendrocytic tissue and a possible inhibition or delay of microglial activation. Disrupted-myelin volume in the DRTZ PNS and CNS compartments of treated tissue was lower, than in control tissue. In the PNS compartment, NT-3 treatment increased phagocyte and blood vessel numbers. It decreased myelinating activity, as sheath thickness was significantly lower and may also account for the noted lower Schwann cell and organelle volume in the test group.


CONCLUSIONS
Our observations suggest that NT-3 interacts with non-neuronal tissue to facilitate the regenerative effort of damaged axons. This may be as a consequence of a direct action or indirectly mediated by modulation of non-neuronal responses to injury.
Department of Anatomy/Neuroscience, BioSciences Institute, National University of Ireland, Cork, Ireland. ahannam@pitt.edu
A T
AT
Hanna-Mitchell
D
D
O'Leary
M S
MS
Mobarak
M S
MS
Ramer
S B
SB
McMahon
J V
JV
Priestley
E N
EN
Kozlova
H
H
Aldskogius
P
P
Dockery
J P
JP
Fraher
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005911:Gliosis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D046529:Microscopy, Electron, Transmission; D009186:Myelin Sheath / Q000187:drug effects / Q000648:ultrastructure; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000502:physiology; D009414:Nerve Growth Factors / Q000494:pharmacology / Q000627:therapeutic use; D009416:Nerve Regeneration / Q000187:drug effects* / Q000502:physiology; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology; D020933:Neurotrophin 3 / Q000494:pharmacology* / Q000627:therapeutic use; D010587:Phagocytosis / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019051:Rhizotomy / Q000009:adverse effects*; D013116:Spinal Cord / Q000187:drug effects* / Q000473:pathology; D013126:Spinal Nerve Roots / Q000187:drug effects* / Q000293:injuries* / Q000473:pathology; D016896:Treatment Outcome; D014855:Wallerian Degeneration / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology
D009414:Nerve Growth Factors; D020933:Neurotrophin 3