Autor: |
Jian-Ping, Yu, Jin, He, Dan, Liu, Chun-Yu, Deng, Xiao-Nan, Zhu, Xue-Lan, Wang, Yong, Wang, Ru-Zhu, Chen |
Rok vydání: |
2007 |
Předmět: |
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Zdroj: |
Sheng li xue bao : [Acta physiologica Sinica]. 59(6) |
ISSN: |
0371-0874 |
Popis: |
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. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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