Journal of Neuroscience, Vol 15, 4133-4139, Copyright © 1995 by Society for Neuroscience
Critical role of the capsaicin-sensitive nerve fibers in the development of the causalgic symptoms produced by transecting some but not all of the nerves innervating the rat tail
YI Kim, HS Na, JS Han and SK Hong
Neuroscience Research Institute, College of Medicine, Korea University, Seoul.
We investigated the role of capsaicin-sensitive small diameter fibers in
the development of the thermal and mechanical allodynia in a new rat model
for neuropathic pain, produced by transecting some but not all of the
nerves innervating the tail. Capsaicin (50 mg/kg, s.c.) injected neonatally
prior to the nerve injury produced thermal hypoalgesia in the tail the
degree of which was variable across individual rats, presumably as a result
of variable degeneration of the small diameter fibers. When subjected to
the nerve injury, the animals with moderate thermal hypoalgesia exhibited
signs of pain (e.g., tail flick) to normally innocuous mechanical stimuli
applied to the tail with von Frey hairs (4.9 mN or 19.6 mN bending force),
but not to thermal stimuli given by immersion of the tail into cold (4
degrees C) or warm (40 degrees C) water. The animals with marked thermal
hypoalgesia, on the other hand, exhibited no signs of pain either to the
mechanical or to the thermal stimuli. These results suggest that the
capsaicin-sensitive fibers are critical in the development of both the
mechanical and thermal allodynia. It is hypothesized that the destruction
of A delta- and C-nociceptive fibers by capsaicin prevented activities
induced in these fibers by the nerve injury from producing a central
sensitization and thus allodynia.
