A non-α7 nicotinic acetylcholine receptor modulates excitatory input to hippocampal CA1 interneurons
A non-α7 nicotinic acetylcholine receptor modulates excitatory input to hippocampal CA1 interneurons
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DOI：
10.1152/jn.00708.2001
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发表时间：
2002-03-01
影响因子：
2.5
通讯作者：
Albuquerque, EX
中科院分区：
文献类型：
--
作者：
Alkondon, M;Albuquerque, EX
烟碱型乙酰胆碱受体（nAChR），特别是α 7亚型，因其在海马锥体神经元以及其他脑区神经元中调节兴奋性突触后电流（EPSC）的作用而受到广泛关注。在这里，我们测试的可能性，nAChR可能会影响EPSC在大鼠海马脑片的中间神经元。采用全细胞膜片钳技术和U型管应用的代理，我们表明，烟碱激动剂增强中间神经元的EPSC频率。在所测试的药剂中，野靛碱和美加明分别是最有效的激动剂和拮抗剂，表明含有α 3 β 4的nAChR在中间神经元EPSC的调节中的作用。对α 7 nAChR具有选择性的配体对中间神经元EPSC的影响非常小或没有影响。低浓度的尼古丁也增强了EPSC频率，暗示非α 7 nAChR参与控制吸烟者的中间神经元兴奋性。我们的结论是，nAChR依赖的EPSC调制在海马是亚型和神经元特异性和非α 7 nAChR，大概是α 3 β 4，控制谷氨酸传输到CA1中间神经元。
The nicotinic acetylcholine receptor (nAChR), particularly the alpha7 subtype, has received profound attention for its role in modifying excitatory postsynaptic currents (EPSCs) in hippocampal pyramidal neurons as well as in neurons from other brain regions. Here, we tested the possibility that an nAChR could affect EPSCs in the interneurons of rat hippocampal slices. Using whole-cell patch-clamp technique on CA1 stratum radiatum interneurons and U-tube application of agents, we show that nicotinic agonists enhance EPSC frequency in interneurons. Among the agents tested, cytisine and mecamylamine were the most effective agonist and antagonist, respectively, suggesting a role for alpha3beta4-containing nAChRs in the modulation of interneuron EPSCs. Ligands selective for the alpha7 nAChR had very little or no effect on interneuron EPSCs. Low concentrations of nicotine also enhanced EPSC frequency, implicating the involvement of non-alpha7 nAChRs in controlling interneuron excitability in smokers. We conclude that nAChR-dependent EPSC modulation in the hippocampus is both subtype- and neuron-specific and that a non-alpha7 nAChR, presumably alpha3beta4, controls glutamate transmission to CA1 interneurons.