Abstract
It was found previously that 1) analgesia measured by tail flick latency of rats, was produced by stimulation of the tibial muscle as an acupuncture point (AP), while was not produced by stimulation of the abdominal muscle as a non-acupuncture point (NAP), 2) analgesia was produced by stimulation of NAP after lesion of the lateral centromedian nucleus of the thalamus (L-CM) or the part of the posterior hypothalamus (I-PH), and 3) AP-stimulation-produced analgesia was abolished by lesion of the dorsal part of the periaqueductal central gray (D-PAG) and NAP-stimulation-produced analgesia was abolished by lesion of the lateral part of the PAG (L-PAG) . In present experiments, the differentiation of the AP and NAP, and the manner of inhibitory action of the analgesia inhibitory system on NAP-stimulation-produced analgesia were examined by recording evoked potential in the D-PAG and L-PAG of rats. Evoked potential was produced in D-PAG by stimulation of AP, not by that of NAP. Evoked potential was produced in the L-PAG by stimulation of both AP and NAP. Stimulation of the L-CM or I-PH with 80 Hz repetitive gradually increasing biphasic train pulses in 600 msec at 1 Hz completely inhibited the L-PAG evoked potential when the recording electrodes were located in the rostral L-PAG and was not inhibited when these were located in the caudal L-PAG. Similar result was obtained in the neuronal activites in the L-PAG produced by NAP stimulation. Evoked potential was produced in the L-CM and I-PH by stimulation of both AP and NAP. The inhibition of the L-PAG evoked potential by I-PH stimulation was abolished by L-CM lesion. L-PAG evoked potential caused by 1 Hz repetitive stimulation of AP or NAP was gradually declined and abolished finally about 10 minutes after stimulation, while D-PAG evoked potential was not influenced by repetitive AP stimulation. Abolition of L-PAG evoked potential by repetitive stimulation of AP or NAP disapperared after lesion of the L-CM. It was concluded that both analgesia producing systen through LPAG and analgesia inhibitory system were activated by stimulation of AP or NAP, while D-PAG was activated only by stimulation of AP. Therefore, analgesia was produced by stimulation of AP but not by stimulation of NAP.
