Differential effects of opioid receptors in nucleus submedius and anterior pretectal nucleus in mediating electroacupuncture analgesia in the rat.
- Author:
Juan-Xia ZHU
1
;
Jing-Shi TANG
;
Hong JIA
Author Information
1. Department of Physiology, School of Medicine, Xi'an Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an 710061, China.
- Publication Type:Journal Article
- MeSH:
Acupuncture Analgesia;
Animals;
Electroacupuncture;
Naloxone;
pharmacology;
Narcotic Antagonists;
Nociceptors;
physiology;
Pain Measurement;
Rats;
Receptors, Opioid;
physiology;
Thalamic Nuclei;
physiology
- From:
Acta Physiologica Sinica
2004;56(6):697-702
- CountryChina
- Language:English
-
Abstract:
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.
