Noradrenaline release by activation of κ-bungarotoxin-sensitive nicotinic acetylcholine receptors participates in long-term potentiation-like response induced by nicotine.
- Author:
Jian-Ping YU
1
;
Jin HE
;
Dan LIU
;
Chun-Yu DENG
;
Xiao-Nan ZHU
;
Xue-Lan WANG
;
Yong WANG
;
Ru-Zhu CHEN
Author Information
1. Experimental Teaching Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Bungarotoxins;
CA1 Region, Hippocampal;
physiology;
Long-Term Potentiation;
drug effects;
Nicotine;
pharmacology;
Norepinephrine;
secretion;
Receptors, Nicotinic;
metabolism
- From:
Acta Physiologica Sinica
2007;59(6):814-820
- CountryChina
- Language:English
-
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 μmol/L) induced LTP-like response in the hippocampal CA1 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 CA1 region in vitro. LTP-like response induced by nicotine was blocked by mecamylamine (1 μmol/L) or κ-bungarotoxin (0.1 μmol/L), but not by dihydro-β-erythtroidine (DHβE, 10 μmol/L). Moreover, it was inhibited by propranolol (10 μmol/L), but not by phentolamine (10 μmol/L) or atropine (10 μmol/L). The results suggest that noradrenaline release secondary to the activation of κ-bungarotoxin-sensitive nAChRs participates in LTP-like response induced by nicotine in the hippocampal CA1 region.
