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首页> 外文期刊>Neuron >Facilitation of long-term potentiation by muscarinic M(1) receptors is mediated by inhibition of SK channels.
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Facilitation of long-term potentiation by muscarinic M(1) receptors is mediated by inhibition of SK channels.

机译：毒蕈碱型M（1）受体的长期增强作用是由抑制SK通道介导的。

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Muscarinic receptor activation facilitates the induction of synaptic plasticity and enhances cognitive function. However, the specific muscarinic receptor subtype involved and the critical intracellular signaling pathways engaged have remained controversial. Here, we show that the recently discovered highly selective allosteric M(1) receptor agonist 77-LH-28-1 facilitates long-term potentiation (LTP) induced by theta burst stimulation at Schaffer collateral synapses in the hippocampus. Similarly, release of acetylcholine by stimulation of cholinergic fibers facilitates LTP via activation of M(1) receptors. N-methyl-D-aspartate receptor (NMDAR) opening during theta burst stimulation was enhanced by M(1) receptor activation, indicating this is the mechanism for LTP facilitation. M(1) receptors were found to enhance NMDAR activation by inhibiting SK channels that otherwise act to hyperpolarize postsynaptic spines and inhibit NMDAR opening. Thus, we describe a mechanism where M(1) receptor activation inhibits SK channels, allowing enhanced NMDAR activity and leading to a facilitation of LTP induction in the hippocampus.
机译：毒蕈碱受体活化促进突触可塑性的诱导并增强认知功能。然而，所涉及的特定毒蕈碱受体亚型和参与的关键细胞内信号传导途径仍存在争议。在这里，我们表明，最近发现的高度选择性的变构M（1）受体激动剂77-LH-28-1促进了由海马Schaffer侧突触的theta爆发刺激引起的长期增强（LTP）。同样，通过刺激胆碱能纤维释放乙酰胆碱通过激活M（1）受体促进LTP。 M（1）受体激活增强了theta爆裂刺激过程中N-甲基-D-天冬氨酸受体（NMDAR）的打开，表明这是LTP促进的机制。 M（1）受体被发现通过抑制SK通道来增强NMDAR激活，否则，SK通道将使突触后棘超极化并抑制NMDAR开放。因此，我们描述了一种机制，其中M（1）受体激活抑制SK通道，允许增强的NMDAR活性并导致海马LTP诱导的促进。

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