Nicotine facilitates long-term potentiation induction in oriens-lacunosum moleculare cells via Ca2+ entry through non-alpha7 nicotinic acetylcholine receptors.
Nicotine facilitates long-term potentiation induction in oriens-lacunosum moleculare cells via Ca2+ entry through non-alpha7 nicotinic acetylcholine receptors.
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DOI：
10.1111/j.1460-9568.2009.07058.x
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发表时间：
2010-02
期刊：
影响因子：
--
通讯作者：
Sumikawa K
中科院分区：
文献类型：
--
作者：
Jia Y;Yamazaki Y;Nakauchi S;Ito K;Sumikawa K
海马抑制性中间神经元在网络活动的控制中具有核心作用，并且它们接收的兴奋性突触表达Hebbian和anti-Hebbian长时程增强（LTP）。由于海马中的许多中间神经元表达烟碱乙酰胆碱受体（nAChRs），我们探讨了暴露于尼古丁是否会促进这些中间神经元的LTP诱导。我们重点关注了东方层/肺泡中的中间神经元子集，由于非脱敏性非α7 nAChR的表达，这些中间神经元在尼古丁存在下持续激活。我们发现，除了α2亚基mRNA外，这些中间神经元还持续表达生长抑素和神经肽Y mRNA，并表现出定向-陷窝细胞的形态特征。非α7 nAChR的激活至少部分地通过Ca 2+通过其通道进入而升高细胞内Ca 2+水平。突触前强直刺激诱导N-甲基-D-天冬氨酸受体非依赖性LTP在电压钳位的中间神经元在−70 mV时，在尼古丁的存在下，但不是没有。细胞内应用的钙离子螯合剂阻断LTP的诱导，这表明LTP的诱导需要钙离子信号。在Ryanodine和L型Ca 2+通道阻断剂硝苯地平的存在下，仍然观察到LTP的诱导，Ryanodine抑制Ca 2+诱导的Ca 2+从Ryanodine敏感的细胞内储存释放。这些结果表明，通过非α7 nAChR通道的Ca 2+内流对于LTP诱导是关键的。因此，尼古丁通过持续激活非α7 nAChR促进定向-腔隙性分子细胞中的LTP诱导，从而影响海马网络活性。
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 focused 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 elevated intracellular Ca2+ levels at least in part via Ca2+ 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 Ca2+ chelator blocked LTP induction, suggesting the requirement of Ca2+ signal for LTP induction. The induction of LTP was still observed in the presence of ryanodine, which inhibits Ca2+-induced Ca2+ release from ryanodine-sensitive intracellular stores, and the L-type Ca2+ channel blocker nifedipine. These results suggest that Ca2+ 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.
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