Fos-immunoreactivity can readily be induced in spinal cord neurones by
noxious, but to a much more limited extent, by innocuous peripheral s
timuli. The present study has investigated whether low intensity stimu
li and electrical stimulation of A beta afferents elicit greater c-fos
expression during the behavioural sensory hypersensitivity generated
by experimental peripheral inflammation. We have examined the time-cou
rse of c-fos expression after inflammation produced by either an intra
-plantar injection of the irritant turpentine oil or of complete Freun
d's adjuvant (CFA). In the former case, a significant initial expressi
on in all dorsal horn laminae was followed by a gradual decrease, wher
eas after CFA injection, an initial expression limited to the superfic
ial laminae subsequently extended into the deep laminae, with a decrea
se at 24 h and an increase in labelling at later times. Low intensity
touch stimuli repeated for 10 min, when applied at 24 h and 48 h after
CFA injection, elicited a significant increase in the number of Fos-i
mmunoreactive neurons in both the superficial and deep laminae of the
dorsal horn compared to non-inflamed animals. Electrical stimulation o
f the sciatic nerve 24 h post-CFA injection, at a strength sufficient
only to activate A beta-afferents fibres (100 mu A, 50 mu s, 10 min),
also elicited a significant increase in labelling relative to the same
stimuli applied in control animals, especially in laminae V-VI. The p
resent results demonstrate that low intensity cutaneous stimuli elicit
a significantly greater increase in c-fos expression in dorsal horn n
eurons during peripheral inflammation and that A beta-afferent input c
ontributes to this, a finding that may relate to the allodynia experie
nced during inflammation.