ABSTRACT
The aim of the present study was to examine whether the thalamic nucleus submedius (Sm) was involved in the modulation of persistent nociception. Using an automated movement detection system to measure nociceptive behavior (agitation) induced by subcutaneous injection of formalin into the hind paw pad, the effects of electrical stimulation or electrolytic lesion of the Sm on the agitation response were examined in conscious rats. Unilateral stimulation (100 μA, 5 min) of the Sm ipsilateral or contralateral to the formalin-injected paw produced a significant inhibition of agitation response in the second phase, while stimulation of thalamic structures more than 0.5 mm away from the Sm had no effect on agitation response. Bilaterally electrolytic lesion of the Sm did not significantly influence the number of agitation events induced by formalin injection in the first phase or the second phase. These results suggest that the Sm is not only involved in the modulation of phase nociception, as reported previously, but also of persistent nociception. The present study provides novel evidence for the participation of the Sm in descending modulation of pain.
Subject(s)
Animals , Rats , Electric Stimulation , Formaldehyde , Nociception , Pain , Pain Measurement , Thalamic NucleiABSTRACT
Previous studies have indicated that the thalamic nucleus submedius (Sm) and the anterior pretectal nucleus (APtN) are involved in the descending modulation of nociception. The aim of the present study was to examine whether the opioid receptors in the Sm and APtN mediated the electroacupuncture (EA)-produced analgesia. The latency of tail flick (TF) reflex induced by radiant heat was used as an index of nociceptive response. The effects of microinjection of opioid receptor antagonist naloxone (1.0 microg, 0.5 ml) into Sm or APtN on the inhibition of the TF reflex induced by EA of "Zusanli" point (St. 36) with high- (5.0 mA) and low- (0.5 mA) intensity were examined in the lightly anesthetized rats. Sm microinjection of naloxone blocked the high- but not low-intensity EA-induced inhibition of the TF reflex. In contrast, naloxone applied to APtN blocked the low- but not high-intensity EA-induced inhibition. When naloxone applied to other brain regions adjacent to Sm or APtN, the EA-induced inhibition was not influenced under either high- or low-intensity condition. These results suggest that opioid receptors in Sm are involved in mediating the analgesia by high-intensity EA for exciting small (A-delta and C group) afferent fibers, while opioid receptors in APtN are involved in mediating the analgesia induced by low-intensity EA for only exciting large (A-beta) afferent fibers.