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WNK3 kinase maintains neuronal excitability by reducing inwardly rectifying K⁺ conductance in layer V pyramidal neurons of mouse medial prefrontal cortex.

ABSTRACT: The with-no-lysine (WNK) family of serine-threonine kinases and its downstream kinases of STE20/SPS1-related proline/alanine-rich kinase (SPAK) and oxidative stress-responsive kinase-1 (OSR1) may regulate intracellular Cl^- homeostasis through phosphorylation of cation-Cl^- co-transporters. WNK3 is expressed in fetal and postnatal brains, and its expression level increases during development. Its roles in neurons, however, remain uncertain. Using WNK3 knockout (KO) mice, we investigated the role of WNK3 in the regulation of the intracellular Cl^- concentration ([Cl^-]_i) and the excitability of layer V pyramidal neurons in the medial prefrontal cortex (mPFC). Gramicidin-perforated patch-clamp recordings in neurons from acute slice preparati

SUBMITTER: Sinha AS

PROVIDER: S-EPMC9613442 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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WNK3 kinase maintains neuronal excitability by reducing inwardly rectifying K⁺ conductance in layer V pyramidal neurons of mouse medial prefrontal cortex.

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Dataset Information

WNK3 kinase maintains neuronal excitability by reducing inwardly rectifying K+ conductance in layer V pyramidal neurons of mouse medial prefrontal cortex.

OmicsDI is part of the ELIXIR infrastructure

Tweets

WNK3 kinase maintains neuronal excitability by reducing inwardly rectifying K⁺ conductance in layer V pyramidal neurons of mouse medial prefrontal cortex.