ArticleEpilepsia2014
Valnoctamide enhances phasic inhibition: a potential target mechanism for the treatment of benzodiazepine-refractory status epilepticus.
Article in Epilepsia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Identifying Drugs that Bind Selectively to Intersubunit General Anesthetic Sites in theMolecular pharmacology · 2019Article
- Valnoctamide Inhibits Cytomegalovirus Infection in Developing Brain and Attenuates Neurobehavioral Dysfunctions and Brain Abnormalities.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Mood stabilizers inhibit cytomegalovirus infection.Virology · 2016Article
- Treatment of Convulsive Status Epilepticus.Current treatment options in neurology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Valnoctamide (VCD), a derivative of valproate, suppresses electrographic seizures in animal models of status epilepticus (SE), even when the seizures are resistant to benzodiazepines (BZDs). We therefore tested the effect of VCD on miniature inhibitory postsynaptic currents (mIPSCs) in CA1 pyramidal cells to determine if VCD acts directly on γ-aminobutyric acid (GABA)A receptors. Bath-applied VCD induced a specific, rapid, dose-dependent, and reversible slowing of the decay of mIPSCs (i.e., increased time constant) with no effect on their frequency or amplitude. This is similar to the effect of BZDs on mIPSCs, but the effect of VCD persisted in the presence of the BZD-binding site antagonist flumazenil, and was additive to the effect of the BZD, diazepam. These data suggest that VCD acts through a different binding site than that of BZDs, which likely accounts for its effect on BZD-refractory SE. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.