Layer-Specific Modulation of the Prefrontal Cortex by Nicotinic Acetylcholine Receptors

Layer-Specific Modulation of the Prefrontal Cortex by Nicotinic Acetylcholine Receptors
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DOI:
10.1093/cercor/bhr390
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发表时间:
2013-01-01
期刊:
影响因子:
3.7
通讯作者:
Mansvelder, Huibert D.
Mansvelder, Huibert D.
中科院分区:
医学2区
文献类型:
--
作者:
Poorthuis, Rogier B.;Bloem, Bernard;Mansvelder, Huibert D.

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乙酰胆碱信号通过烟碱受体(nAChRs)在前额叶皮层(PFC)是至关重要的注意。烟碱性achr在谷氨酸能输入V层细胞、LV中间神经元和LVI锥体神经元上表达。PFC层是否被nachr激活到类似的程度,或者是否存在层特异性激活尚不清楚。在这里,我们研究了nAChR对所有PFC层的调节,并发现锥体神经元具有明显的层特异性:LII/III锥体神经元和谷氨酸能输入不含nAChR, LV和LVI锥体神经元分别由α 7和β 2* nAChR调节。跨层的中间神经元包含nachr的混合组合。然后,我们使用双光子种群成像测试了nachr以层特异性方式激活PFC的假设。在各层中,nachr诱导的神经元放电以β 2* nachr为主。在LII/III中,只有中间神经元被激活。在LV和LVI中,中间神经元和锥体神经元都被激活,后者在LVI中最强烈。总之,这些结果表明,在PFC中,nAChR的激活导致LII/III锥体神经元的抑制。在LV和LVI中,nachr诱导的抑制性和兴奋性神经元的激活导致输出神经元活动的净增强。
Acetylcholine signaling through nicotinic receptors (nAChRs) in the prefrontal cortex (PFC) is crucial for attention. Nicotinic AChRs are expressed on glutamatergic inputs to layer V (LV) cells and on LV interneurons and LVI pyramidal neurons. Whether PFC layers are activated by nAChRs to a similar extent or whether there is layer-specific activation is not known. Here, we investigate nAChR modulation of all PFC layers and find marked layer specificity for pyramidal neurons: LII/III pyramidal neurons and glutamatergic inputs to these cells do not contain nAChRs, LV and LVI pyramidal neurons are modulated by alpha 7 and beta 2* nAChRs, respectively. Interneurons across layers contain mixed combinations of nAChRs. We then tested the hypothesis that nAChRs activate the PFC in a layer-specific manner using 2-photon population imaging. In all layers, nAChR-induced neuronal firing was dominated by beta 2* nAChRs. In LII/III, only interneurons were activated. In LV and LVI, both interneurons and pyramidal neurons were activated, the latter most strongly in LVI. Together, these results suggest that in the PFC nAChR activation results in inhibition of LII/III pyramidal neurons. In LV and LVI, nAChR-induced activation of inhibitory and excitatory neurons results in a net augmentation of output neuron activity.