Noradrenaline release by activation of κ-bungarotoxin-sensitive nicotinic acetylcholine receptors participates in long-term potentiation-like response induced by nicotine / 生理学报
Acta Physiologica Sinica
;
(6): 814-820, 2007.
Article
Dans Anglais
| WPRIM
| ID: wpr-316776
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.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Pharmacologie
/
Physiologie
/
Bungarotoxines
/
Norépinéphrine
/
Récepteurs nicotiniques
/
Potentialisation à long terme
/
Sécrétions corporelles
/
Région CA1 de l'hippocampe
/
Métabolisme
/
Nicotine
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Acta Physiologica Sinica
Année:
2007
Type:
Article
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