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Regulation of Kv4.2 A-Type Potassium Channels in HEK-293 Cells by Hypoxia. | LitMetric

Regulation of Kv4.2 A-Type Potassium Channels in HEK-293 Cells by Hypoxia.

Front Cell Neurosci

Department of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University, Wuhan , China.

Published: October 2014

AI Article Synopsis

  • A-type potassium currents were found to be decreased and neuronal excitability increased in certain brain cells after neonatal hypoxia related to seizures.
  • Research showed that hypoxia led to reduced levels of Kv4.2 channels, which are responsible for these A-type potassium currents, in the hippocampus of neonatal rats.
  • The study concluded that hypoxia directly affects the function of Kv4.2 channels, resulting in decreased current activity, which may contribute to increased neuronal excitability and the tendency for seizures.

Article Abstract

We previously observed that A-type potassium currents were decreased and membrane excitability increased in hippocampal dentate granule cells after neonatal global hypoxia associated with seizures. Here, we studied the effects of hypoxia on the function and expression of Kv4.2 and Kv4.3 α subunit channels, which encode rapidly inactivating A-type K currents, in transfected HEK-293 cells to determine if hypoxia alone could regulate IA in vitro. Global hypoxia in neonatal rat pups resulted in early decreased hippocampal expression of Kv4.2 mRNA and protein with 6 or 12 h post-hypoxia. Whole-cell voltage-clamp recordings revealed that similar times after hypoxia (1%) in vitro decreased peak currents mediated by recombinant Kv4.2 but not Kv4.3 channels. Hypoxia had no significant effect on the voltage-dependencies of activation and inactivation of Kv4.2 channels, but increased the time constant of activation. The same result was observed when Kv4.2 and Kv4.3 channels were co-expressed in a 1:1 ratio. These data suggested that hypoxia directly modulates A-type potassium channels of the subfamily typically expressed in principal hippocampal neurons, and does so in a manner to decrease function. Given the role of IA to slow action potential firing, these data are consistent with a direct effect of hypoxia to decrease IA as a mechanism of increased neuronal excitability and promotion of seizures.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196569PMC
http://dx.doi.org/10.3389/fncel.2014.00329DOI Listing

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