Electroacupuncture (EA) has been successfully used to alleviate
pain produced by various noxious stimulus. Cholecystokinin-8 (CCK-8) is a
neuropeptide involved in the mediation of
pain. We have previously shown that
CCK-8 could antagonize the
analgesic effects of EA on
pain-excited neurons (PENs) and
pain-inhibited neurons (PINs) in the nucleus parafascicularis (nPf). However, its mechanism of action is not clear. In the present study, we applied behavioral and neuroelectrophysiological methods to determine whether the mechanisms of
CCK-8 antagonism to EA
analgesia are mediated through the CCK-A receptors of PENs and PINs in the nPf of rats. We found that focusing radiant heat on the tail of rats caused a simultaneous increase in the evoked discharge of PENs or a decrease in the evoked discharge of PINs in the nPf and the tail-flick reflex. This showed that radiant heat could induce
pain. EA stimulation at the bilateral ST 36
acupoints in rats for 15 min resulted in an inhibition of the electrical activity of PEN, potentiation of the electrical activity of PIN, and prolongation in tail-flick latency (TFL), i.e. EA stimulation produced an
analgesic effect. The
analgesic effect of EA was antagonized when
CCK-8 was injected into the intracerebral ventricle of rats. The antagonistic effect of
CCK-8 on EA
analgesia was reversed by an injection of
CCK-A receptor antagonist
L-364,718 (100 ng/μl) into the nPf of rats. Our results suggest that the
pain-related neurons in the nPf have an important role in mediating EA
analgesia.
L-364,718 potentiates EA
analgesia through the
CCK-A receptor of PENs and PINs in the nPf.