Slack Channels as Key Regulators of Neuronal Excitability: Implications for Neural Function and the Link to Epilepsy Pathogenesis
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Keywords

Slack channel
Neuronal excitability
Epilepsy
Therapeutic strategies

DOI

10.26689/cnr.v2i3.8001

Submitted : 2024-09-02
Accepted : 2024-09-17
Published : 2024-10-02

Abstract

The Slack channel encoded by the KCNT1 gene is a sodium-activated potassium channel. By regulating the flow of potassium ions, the Slack channel affects the membrane potential and discharge activity of neurons, thus participating in regulating neuronal excitability. Therefore, it plays a crucial role in maintaining the normal function of the nervous system. Consequently, abnormal Slack channel function is closely linked to various neurological diseases, such as epilepsy. Currently, quinidine-based medication therapy and neuroregulatory therapy are key components of the treatment of epilepsy resulting from Slack channel dysfunction. This article aims to outline the fundamental features of the Slack channel while providing a thorough analysis of the main distinctions and possible connections between Slick and Slack channels. Furthermore, this study focuses on the function of controlling the neuronal excitability of Slack channels while delving deeper into the potential correlation between Slack channels and epilepsy and their treatment strategies.

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