Study on CCK-8 participated modulation of algesia in caudate nucleus and mechanism of morphine dependence
会议名称:《中国神经科学学会第四次会员代表大会暨第八届全国学术会议》
会议日期:2009年
学科分类:0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
关 键 词:cholecystokinin octapeptide caudate nucleus pain related neuron withdrawal symptom morphine depen- dence
摘 要:正Objective To investigate the effect of caudate nucleus(Cd) on pain transmission and morphine dependence and the influence of cholecystokinin octapeptide(CCK-8) on pain,morphine dependence and withdrawal symptoms. Methods The electrophysiology,morphology and praxiology were used in the ***(1) In normal rats, CCK-8 resulted in increase in the net-increased value(NIV) of evoked discharge frequency,decrease in the average latency of the pain-excitatory neuron(PEN),and prolonged inhibitory duration,reduced the NIV of the pain-inhibitory neuron(PIN).L-365,260,antagonist of CCK-B receptor,antagonized the enhanced effects of PEN,the reduced effects of ***-8 played an excitatory role in the Cd pain transmission in normal rats.(2) Six days after administration of morphine continuously,spontaneous withdrawal symptoms increased obviously during withdrawal 24~72 h in morphinistic *** withdrawal 40h,spontaneous withdrawal symptoms increased much more obviously in morphinistic rats than in normal ones(P0.01).(3) On withdrawal 24h of morphinistic rats,CCK-8 or L-365,260 was injected into the Cd after observed spontaneous withdrawal *** withdrawal 40h,Total score of withdrawal symptoms obviously increased in morphine+CCK-8 rats,and significantly decreased in morphine+L-365,260 rats respectively compared with morphinistic rats group(P0.01).(4) In morphinistic rats,CCK-8 resulted in the increase in the NIV of evoked discharge frequency,the decrease in the average latency of PEN,and prolonged inhibitory duration,reduced the NTV of PIN(P0.05, P0.01).L-365,260 antagonized the enhanced effects of PEN,the reduced effects of ***-8 played an excitatory role in the Cd pain transmission in morphinistic *** Exogenous CCK-8 could potentialize the responses of the pain-related neurons in Cd of normal and morphinism rats to the noxious stimulation,exhibiting the facilitated effect on *** effects of CCK-8 were mainly mediated by CCK-B recept