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Behavior of KCNQ Channels in Neural Plasticity and Motor Disorders

期刊

MEMBRANES
卷 12, 期 5, 页码 -

出版社

MDPI
DOI: 10.3390/membranes12050499

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KCNQ channels; neural plasticity; pain; motor disorders; neurodegenerative disease

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  1. [19AIREA34470007]

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The broad distribution of voltage-gated potassium channels in the human body makes them critical for studying physiological and pathological functions. In neural tissue, KCNQ channels play a significant role in maintaining homeostasis and regulating neural plasticity. Recent research has also highlighted their importance in pharmacotherapeutic and pathological roles, particularly in motor disorders. Understanding the behavior of these channels can provide insights for clinical approaches to chronic pain and guide pharmacotherapeutic developments.
The broad distribution of voltage-gated potassium channels (VGKCs) in the human body makes them a critical component for the study of physiological and pathological function. Within the KCNQ family of VGKCs, these aqueous conduits serve an array of critical roles in homeostasis, especially in neural tissue. Moreover, the greater emphasis on genomic identification in the past century has led to a growth in literature on the role of the ion channels in pathological disease as well. Despite this, there is a need to consolidate the updated findings regarding both the pharmacotherapeutic and pathological roles of KCNQ channels, especially regarding neural plasticity and motor disorders which have the largest body of literature on this channel. Specifically, KCNQ channels serve a remarkable role in modulating the synaptic efficiency required to create appropriate plasticity in the brain. This role can serve as a foundation for clinical approaches to chronic pain. Additionally, KCNQ channels in motor disorders have been utilized as a direction for contemporary pharmacotherapeutic developments due to the muscarinic properties of this channel. The aim of this study is to provide a contemporary review of the behavior of these channels in neural plasticity and motor disorders. Upon review, the behavior of these channels is largely dependent on the physiological role that KCNQ modulatory factors (i.e., pharmacotherapeutic options) serve in pathological diseases.

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