Cholecystokinin octapeptide (CCK-8) has been shown to be a neuropeptide with potent anti-opioid activity. Previous studies have shown that central administration of nanogram dose of CCK-8 totally abolished morphine an...Cholecystokinin octapeptide (CCK-8) has been shown to be a neuropeptide with potent anti-opioid activity. Previous studies have shown that central administration of nanogram dose of CCK-8 totally abolished morphine analgesia in the rat, an effect mediated by CCK-B receptor in central nervous system. In the present study CCK-B antagonist L-365,260 was injected intracerebroventricularly (icv) to Wistar rats to see its effect on the analgesic effect induced by electroacupuncture (EA) stimulation. A marked potentiation of EA-induced analgesia was observed. The degree of potentiation depends on the frequency of EA used, with a rank order of 100 Hz > 15 Hz = 2/15 Hz>> 2Hz. In a strain of rat with acoustically evoked epileptic seizure (P77PMC rats), an extra-ordinarily strong analgesic effect was produced in response to 100 Hz EA stimulation, which was similar to that in Wistar rats pre-treat ed with L-365,260. However, L-365,260 was not effective in potentiating EA analgesia in P77PMC rats. The results suggest that (1) high frequency EA is more likely to increase the release of CCK-8 in CNS as compared to low frequency EA, and (2) P77PMC rats may have a functional defect of the central CCK neurons in the nature of either a low CCK content or a reduced rate of release of CCK-8 in the CNS.展开更多
基金This study was supported by the National Natural Science Foundation of China, and a grant from the National Institute of Drua Abuse, USA (DA 03983).
文摘Cholecystokinin octapeptide (CCK-8) has been shown to be a neuropeptide with potent anti-opioid activity. Previous studies have shown that central administration of nanogram dose of CCK-8 totally abolished morphine analgesia in the rat, an effect mediated by CCK-B receptor in central nervous system. In the present study CCK-B antagonist L-365,260 was injected intracerebroventricularly (icv) to Wistar rats to see its effect on the analgesic effect induced by electroacupuncture (EA) stimulation. A marked potentiation of EA-induced analgesia was observed. The degree of potentiation depends on the frequency of EA used, with a rank order of 100 Hz > 15 Hz = 2/15 Hz>> 2Hz. In a strain of rat with acoustically evoked epileptic seizure (P77PMC rats), an extra-ordinarily strong analgesic effect was produced in response to 100 Hz EA stimulation, which was similar to that in Wistar rats pre-treat ed with L-365,260. However, L-365,260 was not effective in potentiating EA analgesia in P77PMC rats. The results suggest that (1) high frequency EA is more likely to increase the release of CCK-8 in CNS as compared to low frequency EA, and (2) P77PMC rats may have a functional defect of the central CCK neurons in the nature of either a low CCK content or a reduced rate of release of CCK-8 in the CNS.
