Effects of iontophoretic etorphine and naloxone, and electroacupuncture on nociceptive responses from thalamic neurones in rabbits.

A total of 88 somatosensory neurones were recorded from n. anterodorsalis, n. anteroventralis, n. lateralis dorsalis, n. lateralis posterior and n. centralis lateralis of rabbit thalamus. Among the 88 neurones, 50 were noxious-excited (convergent, n = 36; non-convergent with long latency responses, n = 14), 23 noxious-inhibited and 15 non-convergent neurones with short latency responses that were activated by innocuous stimuli only. Iontophoresis of etorphine predominantly depressed the late burst of the response to strong sural nerve stimulation in convergent neurones (25/26), the depression being readily blocked by iontophoresis of naloxone (16/16). After naloxone, the late burst was occasionally larger than that before etorphine. Etorphine depressed non-convergent neurones with long latency responses (13/13), but had no marked effects on non-convergent neurones with short latency responses. On the noxious-inhibited neurones, etorphine could enhance the inhibitory response when it was weak prior to drug administration (12/12). Contrary to etorphine, naloxone could block the inhibitory response when it was administered either iontophoretically (15/15) or intravenously (4/4). Naloxone could enhance the weak late burst of the evoked response in convergent neurones (2/2). Similarly to etorphine, electroacupuncture depressed noxious-excited neurones, convergent (18/18) and non-convergent neurones with long latency responses (6/6), the depression being blocked by naloxone (16/16). The results suggest that noxious inputs may activate the release of opioid peptides onto opiate receptors, the interaction of which mediates the modulation of thalamic nociceptive transmission.

Possible involvement of opioid peptides of caudate nucleus in acupuncture analgesia.

Rabbits chronically implanted with permanent cannulae were used in brain perfusion and microinjection experiments. Potassium iontophoresis applied to the rabbits' ear skin served as a noxious stimulus and the electric current used to elicit the defense response was taken as the pain threshold. The brain perfusate was analysed by radioreceptor assay and the level of endogenous opioid peptides (EOP) was expressed as competition rate. Electroacupuncture (EA) elicited an increase in pain threshold and a rise in EOP level in the perfusate from the anterior part of the head of the caudate nucleus (n = 10, P less than 0.002) but not from the posterior part. The pain threshold raising effect of EA could readily be reversed by microinjection of naloxone into the anterodorsal part of the head of the caudate (n = 12, P less than 0.01). With the techniques of multimicropipettes and microiontophoresis, caudate neuronal activity was recorded and examined in acute animals anesthetized with chloralose and urethane. It was found that microiontophoresed etorphine produced a strong, naloxone reversible inhibition of the spontaneous activity of the caudate neurons (61/162). Most etorphine sensitive neurons were identified in the dorsal part of the head of the caudate (P less than 0.01). EA produced inhibition of some etorphine sensitive neurons (16/35) and the inhibition could also be reversed by microiontophoresis of naloxone (4/8). The results indicate the participation of intracaudate opioid peptides in acupuncture analgesia.