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首页> 外文期刊>Journal of Neurophysiology >Inhibition and disinhibition of pyramidal neurons by activation of nicotinic receptors on hippocampal interneurons.
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Inhibition and disinhibition of pyramidal neurons by activation of nicotinic receptors on hippocampal interneurons.

机译：通过激活海马中间神经元上的烟碱样受体来抑制和抑制锥体神经元。

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Nicotinic acetylcholine receptors (nAChRs) are expressed in the hippocampus, and their functional roles are beginning to be delineated. The effect of nAChR activation on the activity of both interneurons and pyramidal neurons in the CA1 region was studied in rat hippocampal slices. In CA1 stratum radiatum with muscarinic receptors inhibited, local pressure application of acetylcholine (ACh) elicited a nicotinic current in 82% of the neurons. The majority of the ACh-induced currents were sensitive to methyllycaconitine, which is a specific inhibitor of alpha7-containing nAChRs. Methyllycaconitine-insensitive nicotinic currents also were present as detected by a nonspecific nAChR inhibitor. The ACh-sensitive neurons in the s. radiatum were identified as GABAergic interneurons by their electrophysiological properties. Pressure application of ACh induced firing of action potentials in approximately 70% of the interneurons. The ACh-induced excitation of interneurons could induce either inhibition or disinhibition of pyramidal neurons. The inhibition was recorded from the pyramidal neuron as a burst of GABAergic synaptic activity. That synaptic activity was sensitive to bicuculline, indicating that GABA(A) receptors mediated the ACh-induced synaptic currents. The disinhibition was recorded from the pyramidal neuron as a reduction of spontaneous GABAergic synaptic activity when ACh was delivered onto an interneuron. Both the inhibition and disinhibition were sensitive to either methyllycaconitine or mecamylamine, indicating that activation of nicotinic receptors on interneurons was necessary for the effects. These results show that nAChRs are capable of regulating hippocampal circuits by exciting interneurons and, subsequently, inhibiting or disinhibiting pyramidal neurons.
机译：烟碱型乙酰胆碱受体（nAChRs）在海马中表达，其功能作用也开始被描述。在大鼠海马切片中研究了nAChR激活对CA1区中神经元和锥体神经元活性的影响。在具有毒蕈碱受体的CA1辐射层受到抑制的情况下，乙酰胆碱（ACh）的局部压力施加在82％的神经元中引起了烟碱电流。 ACh诱导的电流大多数对甲基lycaconitine敏感，甲基lycaconitine是含α7的nAChRs的特异性抑制剂。如非特异性nAChR抑制剂所检测到的，甲基卡卡尼碱不敏感的烟碱电流也存在。 s中的ACh敏感神经元。放射线通过其电生理特性被鉴定为GABA能中间神经元。施加ACh的压力会引起大约70％的中间神经元触发动作电位。 ACh诱导的中间神经元兴奋可以诱导锥体神经元的抑制或去抑制。从锥体神经元记录的抑制作用是GABA能突触活性的爆发。该突触活性对双小分子敏感，表明GABA（A）受体介导ACh诱导的突触电流。当将ACh传递至中间神经元时，锥体神经元的抑制作用被记录为自发GABA能突触活性降低。抑制作用和去抑制作用均对甲基卡可尼碱或美卡敏敏感，表明中神经元上烟碱样受体的激活对于这种作用是必要的。这些结果表明，nAChRs能够通过激发中间神经元并随后抑制或抑制锥体神经元来调节海马回路。

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