Results 211 to 220 of about 9,333,976 (340)

β‐Hydroxybutyrate reduces neuronal excitability via GIRK channels

open access: yesEpilepsia, EarlyView.
β‐Hydroxybutyrate decreases neuronal excitability by activating GIRK channels through HCAR2 signaling, providing a cellular mechanism that may contribute to the antiseizure effects of the ketogenic diet. Abstract Objective The ketogenic diet is used to treat drug‐resistant epilepsy, yet the molecular mechanisms coupling metabolic state to seizure ...
Soudabeh Naderi   +8 more
wiley   +1 more source

Scn1a‐mediated developmental regulation of prefrontal cortex plasticity and cognition

open access: yesEpilepsia, EarlyView.
Abstract Objective The voltage‐gated sodium channel Nav1.1, encoded by Scn1a, is essential for γ‐aminobutyric acid (GABA)ergic function, and its alteration is associated with neurological disorders such as Dravet syndrome and Alzheimer's disease. We previously demonstrated that local Nav1.1 dysfunction in the medial prefrontal cortex (mPFC) during ...
Maurizio S. Riga   +5 more
wiley   +1 more source

New insights into epileptic spasm generation and treatment from the TTX animal model

open access: yesEpilepsia Open, EarlyView.
Abstract Currently, we have an incomplete understanding of the mechanisms underlying infantile epileptic spasms syndrome (IESS). However, over the past decade, significant efforts have been made to develop IESS animal models to provide much‐needed mechanistic information for therapy development.
John W. Swann   +2 more
wiley   +1 more source

Absence seizures: Update on signaling mechanisms and networks

open access: yesEpilepsia Open, EarlyView.
Abstract Absence seizures (AS) are a hallmark of genetic generalized epilepsies (GGE), characterized by brief episodes of impaired consciousness accompanied by electroencephalographic spike‐and‐wave discharges (SWDs). Traditionally attributed to cortico‐thalamo‐cortical (CTC) dysrhythmia, emerging evidence suggests a more intricate pathophysiological ...
Ozlem Akman, Filiz Onat
wiley   +1 more source

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