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首页> 外文期刊>The European Journal of Neuroscience >Acetylcholine modulates gamma frequency oscillations in the hippocampus by activation of muscarinic M1 receptors
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Acetylcholine modulates gamma frequency oscillations in the hippocampus by activation of muscarinic M1 receptors

机译：乙酰胆碱通过激活毒蕈碱M1受体调节海马中的γ频率振荡

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摘要

Abstract Modulation of gamma oscillations is important for the processing of information and the disruption of gamma oscillations is a prominent feature of schizophrenia and Alzheimer's disease. Gamma oscillations are generated by the interaction of excitatory and inhibitory neurons where their precise frequency and amplitude are controlled by the balance of excitation and inhibition. Acetylcholine enhances the intrinsic excitability of pyramidal neurons and suppresses both excitatory and inhibitory synaptic transmission, but the net modulatory effect on gamma oscillations is not known. Here, we find that the power, but not frequency, of optogenetically induced gamma oscillations in the CA3 region of mouse hippocampal slices is enhanced by low concentrations of the broadspectrum cholinergic agonist carbachol but reduced at higher concentrations. This bidirectional modulation of gamma oscillations is replicated within a mathematical model by neuronal depolarisation, but not by reducing synaptic conductances, mimicking the effects of muscarinic M1 receptor activation. The predicted role for M1 receptors was supported experimentally; bidirectional modulation of gamma oscillations by acetylcholine was replicated by a selective M1 receptor agonist and prevented by genetic deletion of M1 receptors. These results reveal that acetylcholine release in CA3 of the hippocampus modulates gamma oscillation power but not frequency in a bidirectional and dosedependent manner by acting primarily through muscarinic M1 receptors.
机译：摘要伽玛振荡的调制对于加工信息来说是重要的，并且γ振荡的破坏是精神分裂症和阿尔茨海默病的突出特征。通过兴奋性和抑制性神经元的相互作用产生γ振荡，其中通过激发和抑制的平衡来控制它们的精确频率和振幅。乙酰胆碱增强了金字塔神经元的内在兴奋性，抑制了兴奋性和抑制突触差异，但是对γ振荡的净调制效果是不知道的。这里，我们发现，通过低谱曲线胆碱能激动剂卡酚，在小鼠海马切片的CA3区域中的致光学诱导的γ振荡中的功率，但不是频率，但是通过较高的浓度降低。这种双向调制通过神经元去偏振在数学模型中复制，但不是通过降低突触导电，模拟毒蕈碱M1受体活化的影响。实验支持M1受体的预测作用;通过选择性M1受体激动剂复制通过乙酰胆碱的γ振荡的双向调节，并通过M1受体的遗传缺失预防。这些结果表明，通过主要通过毒蕈碱M1受体作用，海马的CA3中的乙酰胆碱释放在海马的CA3中调节γ振荡功率，而不是以双向和依赖性的方式频率。

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