Man Han1, Xiaohua Liu1, Jianqing Du2. 1. Department of Physiology, Shaanxi University of Chinese Medicine, Xianyang 712046, China. 2. Department of Physiology and Pathophysiology, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China.
Abstract
OBJECTIVE: To observe descending inhibition of cardiac nociception induced by microinjection of endomorphin-1 (EM1) in the ventrolateral periaqueductal gray (VLPAG) in rats effect and explore the role of μ-opioid receptor in mediating this effect. METHODS: Male SD rats were randomized into electromyography (EMG) group and c-Fos group, both of which were further divided into 5 subgroups, namely 0.9% NaCl group, bradykinin (BK) group, BK+EM1 group, BK+CTOP group, and BK+CTOP+EM1 group. Rat models of cardiac nociception were established by intrapericardial injection of BK. The changes of cardiaosomatic motor reflex induced by BK were observed by assessing EMG responses of the dorsal spinotrapezius muscle; c-Fos expression in the spinal dorsal horn at levels T3-T5 was tested. RESULTS: Compared with 0.9% NaCl, intrapericardial BK injection induced obvious EMG activities and significantly increased c-Fos expression in the spinal dorsal horn at T3-T5 (P < 0.05). Compared with BK injection, microinjection of EM1 in the VLPAG dose-dependently inhibited EMG activities and significantly decreased c-Fos expression (P < 0.05); microinjection of CTOP in the VLPAG produced no significant effect on EMG or c-Fos expression (P > 0.05). Microinjection of CTOP obviously reversed EM1-induced inhibition of EMG activities and c-Fos expression (P < 0.05). CONCLUSIONS: Microinjection of EM1 in the VLPAG produces descending inhibition of cardiac nociception in rats by activating μ-opioid receptor.
OBJECTIVE: To observe descending inhibition of cardiac nociception induced by microinjection of endomorphin-1 (EM1) in the ventrolateral periaqueductal gray (VLPAG) in rats effect and explore the role of μ-opioid receptor in mediating this effect. METHODS: Male SD rats were randomized into electromyography (EMG) group and c-Fos group, both of which were further divided into 5 subgroups, namely 0.9% NaCl group, bradykinin (BK) group, BK+EM1 group, BK+CTOP group, and BK+CTOP+EM1 group. Rat models of cardiac nociception were established by intrapericardial injection of BK. The changes of cardiaosomatic motor reflex induced by BK were observed by assessing EMG responses of the dorsal spinotrapezius muscle; c-Fos expression in the spinal dorsal horn at levels T3-T5 was tested. RESULTS: Compared with 0.9% NaCl, intrapericardial BK injection induced obvious EMG activities and significantly increased c-Fos expression in the spinal dorsal horn at T3-T5 (P &lt; 0.05). Compared with BK injection, microinjection of EM1 in the VLPAG dose-dependently inhibited EMG activities and significantly decreased c-Fos expression (P &lt; 0.05); microinjection of CTOP in the VLPAG produced no significant effect on EMG or c-Fos expression (P &gt; 0.05). Microinjection of CTOP obviously reversed EM1-induced inhibition of EMG activities and c-Fos expression (P &lt; 0.05). CONCLUSIONS: Microinjection of EM1 in the VLPAG produces descending inhibition of cardiac nociception in rats by activating μ-opioid receptor.