ArticleJournal of molecular neuroscience : MN2015
Elevated Expression of the Delta-Subunit of Epithelial Sodium Channel in Temporal Lobe Epilepsy Patients and Rat Model.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 3 citations in OpenAlex.
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6 authors at 2 institutions in 1 country.
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Abstract
Epilepsy is one of the most common, chronic, neurological diseases. The pathology of epilepsy is based on abnormal synchronization of neuronal discharges. Epithelial sodium channels, which are constitutively active, non-voltage-gated, highly selective sodium channels belonging to the epithelial sodium channel/degenerin (ENaC/deg) family, contribute to resting membrane potential modulation and subsequent neuronal excitability by providing a sodium influx pathway. Different from the other three subunits, δ ENaC expression is prominent in the human brain cortex and restricted to neurons. The aim of this study was to investigate the expression pattern of δ ENaC in patients with temporal lobe epilepsy (TLE) and in a pilocarpine-induced rat model of epilepsy. Adopting immunohistochemistry, immunofluorescence, and western blot analysis, we found that δ ENaC was restricted to neurons in the temporal neocortices of TLE patients and the cortices and hippocampus of pilocarpine-induced epilepsy rats, which were similar to the corresponding controls. However, δ ENaC expression was significantly elevated in TLE patients and the pilocarpine-induced epileptic rats. The physiological role, the unchanged localization, and the elevated expression of δ ENaC suggested it could play an important role in epilepsy.
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