Noradrenaline release by activation of #kappa#--bungarotoxin--sensitive nicotinic acetylcholine receptors participates in long--term potentiation--like response induced by nicotine
Yu Jianping, He Jin, Liu Dan, Deng Chunyu, Zhu Xiaonan, Wang Xuelan, Wang Yong, Chen Ruzhu
Experimental Teaching Center,Zhongshan School of Medicine, Sun Yat-Sen University.Guangzhou 510080,Guangdong;China;Research Center of Medical Sciences, Guangdong Provincial People's Hospital.Guangzhou 510080,Guangdong;Depar
Abstract
Nicotine enhances the function of learning and memory, but the underlying mechanism still remains unclear. Hippocampal long-term potentiation (LTP) is assumed to be a cellular mechanism of learning and memory. Our previous experiments showed that with the single pulses evoking 80% of the maximal population spike (PS) amplitude, nicotine (10 #mu#mol/L) induced LTP-like response in the hippocampal CAI region. In the present study, the nicotinic acetylcholine receptor (nAChR) subtypes and relevant neurotransmitter releases involved in LTP-like response induced by nicotine were investigated by extracellularly recording the PS in the pyramidal cell layer in the hippocampal CAI region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine (1 #mu#mol/L) or #kappa#-bungarotoxin (0.1 #mu#mol/L), but not by dihydro-#beta#-erythtroidine (DH#beta#E, 10 #mu#mol/L). Moreover, it was inhibited by propranolol (10 #mu#mol/L), but not by phentolamine (10 #mu#mol/L) or atropine (10 #mu#mol/L). The results suggest that noradrenaline release secondary to the activation of #beta#-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CAI region.
Key words: Long-term potentiation;#kappa#-bungarotoxin;nicotinic acetylcholine receptors;Noradrenaline;Hippocampus
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Citing This Article:
Yu Jianping, He Jin, Liu Dan, Deng Chunyu, Zhu Xiaonan, Wang Xuelan, Wang Yong, Chen Ruzhu. Noradrenaline release by activation of #kappa#--bungarotoxin--sensitive nicotinic acetylcholine receptors participates in long--term potentiation--like response induced by nicotine. Acta Physiol Sin 2007; 59 (6): 814-820 (in Chinese with English abstract).