Calcium-activated chloride channels (CaCCs) regulate action potential and synaptic response in hippocampal neurons.
Calcium-activated chloride channels (CaCCs) regulate action potential and synaptic response in hippocampal neurons.
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DOI：
10.1016/j.neuron.2012.01.033
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发表时间：
2012-04-12
期刊：
影响因子：
16.2
通讯作者：
Jan LY
中科院分区：
文献类型：
--
作者：
Huang WC;Xiao S;Huang F;Harfe BD;Jan YN;Jan LY
中枢神经元通过产生突触电位来响应来自其他神经元的突触输入。一旦总的突触电位达到动作电位激发的阈值，信号就会传播，导致突触释放递质。伴随着这种信号的钙内流打开了钙激活的离子通道以进行反馈调节。在这里，我们报道了一种新的机制来调节海马神经元信号，涉及钙激活的氯通道(CaCC)。我们首次提出了CaCCs存在于海马神经元中，并与钙通道和NMDA受体紧密相连的证据，以缩短动作电位时程，抑制兴奋性突触电位，阻止时间总和，并提高突触电位产生动作电位的阈值。在最近确定TMEM16A和TMEM16B为CaCC之后，我们进一步证明TMEM16B而不是TMEM16A对海马CACC是重要的，为破译CACC对学习和记忆重要的神经元中神经元信号的动态调制奠定了基础。
Central neurons respond to synaptic inputs from other neurons by generating synaptic potentials. Once the summated synaptic potentials reach threshold for action potential firing, the signal propagates leading to transmitter release at the synapse. The calcium influx accompanying such signaling opens calcium-activated ion channels for feedback regulation. Here we report a novel mechanism for modulating hippocampal neuronal signaling that involves calcium-activated chloride channels (CaCCs). We present the first evidence that CaCCs reside in hippocampal neurons and are in close proximity of calcium channels and NMDA receptors to shorten action potential duration, dampen excitatory synaptic potentials, impede temporal summation, and raise the threshold for action potential generation by synaptic potential. Having recently identified TMEM16A and TMEM16B as CaCCs, we further show that TMEM16B but not TMEM16A is important for hippocampal CaCC, laying the groundwork for deciphering the dynamic CaCC modulation of neuronal signaling in neurons important for learning and memory.
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