Article

Spasticity and allodynia are major sequelae that affect the quality
of life and daily activities of spinal cord injury (SCI) patients. Although
rehabilitation ameliorates spasticity and allodynia, the molecular mechanisms
involved in these processes remain elusive. OBJECTIVE: To investigate the
molecular mechanisms by which rehabilitation ameliorates spasticity and allodynia
after SCI in rats. METHODS: The expression levels of brain-derived neurotrophic
factor (BDNF) and potassium-chloride cotransporter-2 (KCC2), as well as the
localization of KCC2, were examined in the lumbar enlargements of untrained and
treadmill-trained thoracic SCI model rats. Spasticity and allodynia were
determined via behavioral and electrophysiological analyses. The effects of BDNF
on spasticity, allodynia, and KCC2 activation were determined by inhibition of
BDNF signaling via intrathecal administration of TrkB-IgG. The effects of SCI and
training on the expression levels of functional phospholipase C-gamma in the
lumbar enlargement were also examined. RESULTS: Treadmill training after SCI
upregulated endogenous BDNF expression and posttranslational modification of KCC2
in the lumbar enlargement significantly. There were also significant correlations
between increased KCC2 expression and ameliorated spasticity and allodynia.
Administration of TrkB-IgG abrogated the training-induced upregulation of KCC2
and beneficial effects on spasticity and allodynia. The expression level of
functional phospholipase C-gamma was reduced significantly after SCI, which may
have contributed to the change in the function of BDNF, whereby it did not trigger short-term downregulation or induce long-term upregulation of KCC2
expression secondary to training. CONCLUSIONS: BDNF-mediated restoration of KCC2
expression underlies the suppression of spasticity and allodynia caused by
rehabilitation.
CI - (c) The Author(s) 2014.

Langue : ANGLAIS