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Vol. 297, Issue 3, 1210-1217, June 2001
Departments of Pharmacology and Toxicology (S.M.S., J.A.D.) and
Anesthesiology (J.A.D.), Dartmouth College, Hanover, New Hampshire; and
Department of Neuromorphology, Max-Planck-Institute of Neurobiology,
Martinsried, Germany (P.S.)
The present study was undertaken to determine whether propentofylline,
a glial modulating agent, could both prevent the induction of
mechanical allodynia and attenuate existing mechanical allodynia in a
rodent L5 spinal nerve transection model of neuropathic pain. In a
preventative paradigm, propentofylline (1 and 10 mg/kg
intraperitoneally) was administered systemically daily, beginning 1 day
prior to nerve transection. This regimen produced a dose-dependent
decrease in mechanical allodynia (p < 0.01). In
another preventative paradigm, propentofylline (0.1, 1, or 10 µg) was
administered daily intrathecally via direct lumbar puncture.
Intrathecal administration of propentofylline was more effective than
systemic administration at dose dependently reducing mechanical
allodynia (p < 0.01). The effect of systemic propentofylline on existing allodynia was examined with 0.1-, 1-, and
10-mg/kg intraperitoneal administration initiated on day 4 post L5
spinal nerve transection. Systemic propentofylline was found to be
equally effective in the attenuation of existing allodynia (p < 0.01) as in the prevention of allodynia in
this rodent model of neuropathic pain. Spinal cords (L4-L6 segments)
were removed for immunohistochemical analysis on day 10 or 20 post-transection. Microglial and astrocytic activation was decreased by
both peripheral and central administration of propentofylline in both
preventative and existing allodynia paradigms. This research supports a
growing body of literature highlighting the importance of glial
activation in the development of persistent neuropathic pain states,
and the potential to therapeutically modulate glial activation in the
treatment of neuropathic pain.
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