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首页> 外文期刊>Neuron >M1 muscarinic receptors boost synaptic potentials and calcium influx in dendritic spines by inhibiting postsynaptic SK channels.
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M1 muscarinic receptors boost synaptic potentials and calcium influx in dendritic spines by inhibiting postsynaptic SK channels.

机译：M1毒蕈碱受体通过抑制突触后SK通道来增强树突棘的突触电位和钙内流。

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摘要

Acetylcholine release and activation of muscarinic cholinergic receptors (mAChRs) enhance synaptic plasticity in vitro and cognition and memory in vivo. Within the hippocampus, mAChRs promote NMDA-type glutamate receptor-dependent forms of long-term potentiation. Here, we use calcium (Ca) imaging combined with two-photon laser glutamate uncaging at apical spines of CA1 pyramidal neurons to examine postsynaptic mechanisms of muscarinic modulation of glutamatergic transmission. Uncaging-evoked excitatory postsynaptic potentials and Ca transients are increased by muscarinic stimulation; however, this is not due to direct modulation of glutamate receptors. Instead, mAChRs modulate a negative feedback loop in spines that normally suppresses synaptic signals. mAChR activation reduces the Ca sensitivity of small conductance Ca-activated potassium (SK) channels that are found in the spine, resulting in increased synaptic potentials and Ca transients. These effects are mediated by M1-type muscarinic receptors and occur in a casein kinase-2-dependent manner. Thus, muscarinic modulation regulates synaptic transmission by tuning the activity of nonglutamatergic postsynaptic ion channels.
机译：乙酰胆碱的释放和毒蕈碱型胆碱能受体（mAChRs）的活化可在体外增强突触可塑性，并在体内增强认知和记忆能力。在海马中，mAChRs促进NMDA型谷氨酸受体依赖性长期增强。在这里，我们使用钙（Ca）成像结合在CA1锥体神经元的顶棘开松的两光子激光谷氨酸释放，以检查味精对谷氨酸能传递的突触后机制。毒蕈碱刺激会增加未笼诱发的兴奋性突触后电位和Ca瞬变。然而，这不是由于谷氨酸受体的直接调节。取而代之的是，mAChR调节脊柱中的负反馈回路，该回路通常会抑制突触信号。 mAChR激活降低了在脊柱中发现的小电导Ca激活的钾（SK）通道的Ca敏感性，导致突触电位和Ca瞬变增加。这些作用是由M1型毒蕈碱受体介导的，并以酪蛋白激酶2依赖性方式发生。因此，毒蕈碱调节通过调节非谷氨酸能突触后离子通道的活性来调节突触传递。

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