• Neuromodulation · Apr 2010

    Cholecystokinin-8 antagonizes electroacupuncture analgesia through its B receptor in the caudate nucleus.

    • Chun-Xiao Yang, Tie-Feng Shi, Qing-Cheng Liang, Bao-Feng Yang, Run-Sheng Jiao, Hui Zhang, Ying Zhang, and Man-Ying Xu.
    • Department of Neurology of 2nd Affiliated Hospital, Harbin, Heilongjiang Province, China; College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang Province, China; and Laboratory of Neural Electrophysiology, Department of Physiology, Harbin Medical University, Harbin, Heilongjiang Province, China.
    • Neuromodulation. 2010 Apr 1;13(2):93-8.

    Objectives  The analgesic effect of electroacupuncture (EA) stimulation has been proved. However, its mechanism of action is not clear. It has been well-known that cholecystokinin-8 (CCK-8) is a neuropeptide which is mainly related to the mediation of pain. The caudate nucleus was selected to determine if the release of CCK and the neural activity in this nucleus were involved in producing EA analgesia.Materials And Methods  Radiant heat focused on the rat-tail was used as the noxious stimulus. The pain threshold of rats was measured by tail-flick latency (TFL). EA stimulation at the bilateral Zusanli (ST 36) acupoints of rats was used to investigate the effects of EA analgesia. The electrical activities of pain-excited neurons (PEN) and pain-inhibited neurons (PIN) in the caudate nucleus were recorded with a glass microelectrode. The present study examined the antagonistic effects of the intracerebral ventricular injection of CCK-8 on EA analgesia and reversing effects of CCK-B receptor antagonist (L-365,260) injection into the caudate nucleus on CCK-8.Results  The radiant heat focused on the tail of rats caused an increase in the evoked discharge of PEN and a reduction in the evoked discharge of PIN. EA stimulation at the bilateral ST 36 acupoints of rats resulted in the inhibition of PEN, the potentiation of PIN, and prolongation of TFL. The analgesic effect of EA was antagonized when CCK-8 was injected into the intracerebral ventricle of rats. The antagonistic effect of CCK-8 on EA analgesia was reversed by injection of CCK-B receptor antagonist (L-365,260) into the caudate nucleus of rats.Conclusions  Our results suggest that CCK-8 antagonize EA analgesia through its B receptor.© 2009 International Neuromodulation Society.

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