Cheng Huanga, Yun Wanga,*, Jaw-Kang Changb, Ji-Sheng Hana
aNeuroscience Research Institute, Peking University, 38 Xue Yuan Road, Beijing 100083, PR China
bPhoenix Pharmaceuticals Inc., California, CA, USA
Received 24 August 2000; received in revised form 5 October 2000; accepted 6 October 2000
Abstract
This work was designed to examine whether brain endomorphins (EM1 and EM2), the endogenous m-opioid ligands,are involved in electroacupuncture (EA)-induced analgesia in the mice. C57BL/6J mice were given EA for 30 min and the effect of EA-induced analgesia was assessed by radiant heat tail ¯ick latency (TFL). Intracerebroventricular (i.c.v.) injection of m-opioid receptor antagonist D-Phe-Cys-Tyr-D-Tyr-Orn-Thr-Pen-Thr-NH2 (CTOP), or antiserum against EM1 or
EM2 was performed to see whether EA analgesia could be blocked. The results showed that: (1) i.c.v. injection of CTOP at 25±100 ng dose-dependently antagonized the analgesia induced by EA of 2 Hz, but not 100 Hz. (2) Intracerebroventricular injection of EM1 antiserum (5 ml, 1:1 or 1:10 dilution) dose-dependently antagonized 2 Hz, but not 100 Hz EA analgesia. (3) EM2 antiserum showed similar effect at 1:1 dilution. The results are interpreted to mean that endogenously released EM1 and EM2 and the cerebral m-receptors are involved in mediating 2 Hz but not 100 Hz EA analgesia in the mice.
q 2000 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Endomorphin; m-Opioid receptor; Receptor antagonist; Analgesia; Antiserum; Electroacupuncture
