Neuronal firing patterns and frequencies determine the nature of encoded information of the neurons. Here we discuss the molecular identity and cellular mechanisms of spike-frequency adaptation in central nervous system (CNS) neurons. Calcium-activated potassium (K_Ca) channels such as BK_Ca and SK_Ca channels have long been known to be important mediators of spike adaptation via generation of a large afterhyperpolarization when neurons are hyper-activated. However, it has been shown that a strong hyperpolarization via these K_Ca channels would cease action potential generation rather than reducing the frequency of spike generation. In some types of neurons, the strong hyperpolarization is followed by oscillatory activity in these neurons. Recently, spike-frequency adaptation in thalamocortical (TC) and CA1 hippocampal neurons is shown to be mediated by the Ca²⁺-activated Cl- channel (CACC), anoctamin-2 (ANO2). Knockdown of ANO2 in these neurons results in significantly reduced spike-frequency adaptation accompanied by increased number of spikes without shifting the firing mode, which suggests that ANO2 mediates a genuine form of spike adaptation, finely tuning the frequency of spikes in these neurons. Based on the finding of a broad expression of this new class of CACC in the brain, it can be proposed that the ANO2-mediated spike-frequency adaptation may be a general mechanism to control information transmission in the CNS neurons.

中文翻译：

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中枢神经系统神经元的峰值频率适应。

神经元放电模式和频率决定了神经元编码信息的性质。在这里，我们讨论中枢神经系统（CNS）神经元的峰频率适应的分子身份和细胞机制。长期以来，人们一直知道钙激活的钾（K _Ca）通道（例如BK _Ca和SK _Ca通道）是神经元被过度激活时通过产生大的超极化后超极化的信号，从而成为尖峰适应的重要介体。然而，已经显示出通过这些K _Ca的强超极化作用。通道将停止动作电位的产生，而不是减少尖峰产生的频率。在某些类型的神经元中，强超极化之后是这些神经元中的振荡活动。最近，显示丘脑皮层（TC）和CA1海马神经元的峰频率适应是由Ca ²⁺介导的激活的Cl-通道（CACC），octamin-2（ANO2）。敲低这些神经元中的ANO2会导致尖峰频率适应性显着降低，同时伴随增加的尖峰数量而不会改变触发模式，这表明ANO2介导了一种真正的尖峰适应形式，可以精细调节这些神经元中的尖峰频率。基于在大脑中这种新型CACC广泛表达的发现，可以提出ANO2介导的尖峰频率适应可能是控制CNS神经元信息传递的通用机制。