Small conductance calcium-activated potassium channels (SKs) are solely activated by intracellular Ca²⁺ and their activation leads to potassium efflux, thereby repolarizing/hyperpolarizing membrane potential. Thus, these channels play a critical role in synaptic transmission, and consequently in information transmission along the neuronal circuits expressing them. SKs are widely but not homogeneously distributed in the central nervous system (CNS). Activation of SKs requires submicromolar cytoplasmic Ca²⁺ concentrations, which are reached following either Ca²⁺ release from intracellular Ca²⁺ stores or influx through Ca²⁺ permeable membrane channels. Both Ca²⁺ sensitivity and synaptic levels of SKs are regulated by protein kinases and phosphatases, and degradation pathways. SKs in turn control the activity of multiple Ca²⁺ channels. They are therefore critically involved in coordinating diverse Ca²⁺ signaling pathways and controlling Ca²⁺ signal amplitude and duration. This review highlights recent advances in our understanding of the regulation of SK2 channels and of their roles in normal brain functions, including synaptic plasticity, learning and memory, and rhythmic activities. It will also discuss how alterations in their expression and regulation might contribute to various brain disorders such as Angelman Syndrome, Alzheimer's disease and Parkinson's disease.

小电导钙激活钾通道 (SK) 仅由细胞内 Ca ²⁺激活，它们的激活导致钾外流，从而使膜电位复极化/超极化。因此，这些通道在突触传递中起着关键作用，因此在沿着表达它们的神经元回路的信息传递中起着关键作用。SK 广泛但不均匀分布在中枢神经系统 (CNS) 中。SKs 的激活需要亚微摩尔的细胞质 Ca ²⁺浓度，该浓度是在 Ca ²⁺从细胞内 Ca ²⁺储存库释放或通过 Ca ²⁺渗透膜通道流入后达到的。两者 Ca ²⁺SKs 的敏感性和突触水平受蛋白激酶和磷酸酶以及降解途径的调节。SK 反过来控制多个 Ca ²⁺通道的活性。因此，它们在协调不同的 Ca ²⁺信号通路和控制 Ca ²⁺信号幅度和持续时间方面至关重要。这篇综述强调了我们对 SK2 通道调节及其在正常大脑功能（包括突触可塑性、学习和记忆以及节律活动）中的作用的理解的最新进展。它还将讨论它们的表达和调节的改变如何导致各种脑部疾病，如天使综合症、阿尔茨海默病和帕金森病。