Jw. Hu et al., OPIOID INVOLVEMENT IN ELECTROMYOGRAPHIC (EMG) RESPONSES INDUCED BY INJECTION OF INFLAMMATORY IRRITANT INTO DEEP NECK TISSUES, Somatosensory & motor research, 13(2), 1996, pp. 139-146
Previously, we have demonstrated (Hu et al., 1993) that injection of t
he small-fiber excitant and inflammatory irritant mustard oil (MO) int
o deep paraspinal tissues surrounding C-1-C-2 vertebrae can evoke a su
stained and reversible increase of electromyographic (EMG) activity of
neck and jaw muscles, and can also produce an acute inflammatory resp
onse. This increased EMG activity lasts up to 20 min; within 30 min fo
llowing MO injection, the activity returns to preinjection levels. The
aim of our present study was to determine whether an opioid suppressi
ve mechanism may be involved in limiting the increased EMG activity, d
espite the presence of an ongoing inflammatory response. Three doses (
0.6 mg/kg, 1.2 mg/kg, and 2.5 mg/kg) of the opioid antagonist naloxone
, along with vehicle (saline), were administered intravenously to dete
rmine whether naloxone is capable of inducing a significant recurrence
(''rekindling'' effect) of EMG activity. A dose-dependent process in
the naloxone-induced rekindling effect was demonstrated for the area u
nder the curve of rectified and integrated EMG activity. At the highes
t dose (2.5 mg/kg), the relative area of naloxone-evoked EMG activity
increases reached 83% of the original MO-induced EMG activity level. T
hese results suggest that a central opioid suppressive mechanism is ac
tivated by the MO-induced small-afferent barrage, and that this may li
mit the duration and magnitude of the evoked EMG changes.