k-银环蛇毒素敏感的烟碱受体激活引起的去甲肾上腺素释放参与烟碱诱导的长时程增强样反应.pdfVIP

814 Acta Physiologica Sinica， December 25，2007，59(6)：8 14-820 http：／／www．actaps．com．cn Noradrenaline release by activation of~-bungarotoxin·sensitive nicotinic acetylcholin(receptors participates in long term potentiation．1ik,ac lcho ne partlclpates in lon2-term Dote ● like ● l l ● - ● respouse induced Dy mcot-me YU Jian—Ping ，HE Jin。，LIU Dan4，DENG Chun一 ，u。，ZHU Xiao-Nan。， NG Xue—Lan。，W：A NG Yong ， CHEN Ru—Zhu2， Experimental Teaching Center；：Department ofPharmacology,Zhongshan School ofMedicine，Sun Yat—Sen University,Guangzhou 510080,China；3Research Center ofMedical Sciences。Guangdong Provincial People S Hospital,Guangzhou 5lo08o1 China； Laboratory ofPharmaceutical Analysis and Quality Evaluation,School ofPharmaceutical Sciences,Sun Yat—Sen University, Guangzhou 510080,China；5Department of Clinical Pharmacology ofZhufiang Hospital,Southern Medical University,Guangzhou 5lo282．China Abstract：Nicotine enhances the function of learning and memory，but the underlying mechanism still remains unclear．Hippocampal long—term potentiation(UrP)is assumed to be a cellular mechanism of learning and memory．Our previous experiments showed that with the single pulses evoking 80％ofthe maximal population spike(PS)amplitude，nicotine(10 larnol／L)induced UrP-like response in the hippocampal CAI region．In the present study，the nicotinic acetylcholine receptor(nAChR)subtypes and relevant neuroffans— mitter releases involved in m —like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CAI region in vitro．UrI)-like response induced by nicotine was blocked by mecamylamine(1 prnol／L)or K-bungarotoxin(0．1 I~rnol／L)，but not by dihydro—B-erythtroidine(DHBE，10 prnol／L)．Moreover，it was inhibited by propranolol(