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Readable research linked to original sources
Browse normalized, publication-ready research with direct links to its evidence and source.
Loading articles data…
Readable research linked to original sources
Browse normalized, publication-ready research with direct links to its evidence and source.
5 articles
Newest firstBackground Chronic pain, which is often unrelated to ongoing injury, is poorly understood and difficult to treat. Genetic studies have identified voltage-gated sodium (Nav) channels, particularly gain-of-function mutations such as L858F and R1150W in human NaV1.7, as involved in the development of chronic pain. Methods A chronic pain model was proposed in Drosophila using the parabss1 mutant. Behavioural chemical…
Open article record in new tab ↗Objective To investigate the anti-inflammatory properties of anti-seizure medications (ASMs) administered to patients with drug-resistant epilepsy (DRE) and the role of sodium channels in microglial activation. Material Primary microglia monocultures from mice brains. Treatment Microglia were activated with 10 μg/mL lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (poly I:C) and pre- (45 min ASM then 2…
Persistent sodium current (INaP) is an important activity-dependent regulator of neuronal excitability. It is involved in a variety of physiological and pathological processes, including pacemaking, prolongation of sensory potentials, neuronal injury, chronic pain and diseases such as epilepsy and amyotrophic lateral sclerosis. Despite its importance, neither the molecular basis nor the regulation of INaP are suff…
Open article record in new tab ↗Cannabidiol (CBD), a major non-psychoactive phytocannabinoid in cannabis, is an effective treatment for some forms of epilepsy and pain. At high concentrations, CBD interacts with a huge variety of proteins, but which targets are most relevant for clinical actions is still unclear. Here we show that CBD interacts with Nav1.7 channels at sub-micromolar concentrations in a state-dependent manner. Electrophysiologica…
Open article record in new tab ↗Background Cerebral overexcitation needs inhibitory neurons be functionally upregulated to rebalance excitation vs. inhibition. For example, the intensive activities of GABAergic neurons induce spontaneous spikes, i.e., activity-induced spontaneous spikes (AISS). The mechanisms underlying AISS onset remain unclear. We investigated the roles of sodium channels in AISS induction and expression at hippocampal GABAerg…
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