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Nicotine facilitates long‐term potentiation induction in oriens‐lacunosum moleculare cells via Ca 2+ entry through non‐α7 nicotinic acetylcholine receptors
Author(s) -
Jia Yousheng,
Yamazaki Yoshihiko,
Nakauchi Sakura,
Ito KenIchi,
Sumikawa Katumi
Publication year - 2010
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2009.07058.x
Subject(s) - long term potentiation , neuroscience , nicotinic agonist , nicotine , acetylcholine receptor , term (time) , chemistry , acetylcholine , receptor , psychology , biology , pharmacology , physics , biochemistry , quantum mechanics
Hippocampal inhibitory interneurons have a central role in the control of network activity, and excitatory synapses that they receive express Hebbian and anti‐Hebbian long‐term potentiation (LTP). Because many interneurons in the hippocampus express nicotinic acetylcholine receptors (nAChRs), we explored whether exposure to nicotine promotes LTP induction in these interneurons. We focussed on a subset of interneurons in the stratum oriens/alveus that were continuously activated in the presence of nicotine due to the expression of non‐desensitizing non‐α7 nAChRs. We found that, in addition to α2 subunit mRNAs, these interneurons were consistently positive for somatostatin and neuropeptide Y mRNAs, and showed morphological characteristics of oriens‐lacunosum moleculare cells. Activation of non‐α7 nAChRs increased intracellular Ca 2+ levels at least in part via Ca 2+ entry through their channels. Presynaptic tetanic stimulation induced N ‐methyl‐ d ‐aspartate receptor‐independent LTP in voltage‐clamped interneurons at −70 mV when in the presence, but not absence, of nicotine. Intracellular application of a Ca 2+ chelator blocked LTP induction, suggesting the requirement of Ca 2+ signal for LTP induction. The induction of LTP was still observed in the presence of ryanodine, which inhibits Ca 2+ ‐induced Ca 2+ release from ryanodine‐sensitive intracellular stores, and the L‐type Ca 2+ channel blocker nifedipine. These results suggest that Ca 2+ entry through non‐α7 nAChR channels is critical for LTP induction. Thus, nicotine affects hippocampal network activity by promoting LTP induction in oriens‐lacunosum moleculare cells via continuous activation of non‐α7 nAChRs.