ArticleBMC neurology2012
4-Chloropropofol enhances chloride currents in human hyperekplexic and artificial mutated glycine receptors.
Article in BMC neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Glycine receptors and glycine transporters: targets for novel analgesics?Cellular and molecular life sciences : CMLS · 2018Review
- Activation and modulation of recombinant glycine and GABABritish journal of pharmacology · 2016Article
- Phosphorylation state-dependent modulation of spinal glycine receptors alleviates inflammatory pain.The Journal of clinical investigation · 2016Article
- 4-bromopropofol decreases action potential generation in spinal neurons by inducing a glycine receptor-mediated tonic conductance.British journal of pharmacology · 2014Article
- Comparative pharmacology of flatworm and roundworm glutamate-gated chloride channels: Implications for potential anthelmintics.International journal for parasitology. Drugs and drug resistance · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe mammalian neurological disorder hereditary hyperekplexia can be attributed to various mutations of strychnine sensitive glycine receptors. The clinical symptoms of "startle disease" predominantly occur in the newborn leading to convulsive hypertonia and an exaggerated startle response to unexpected mild stimuli. Amongst others, point mutations R271Q and R271L in the α1-subunit of strychnine sensitive glycine receptors show reduced glycine sensitivity and cause the clinical symptoms of hyperekplexia.Halogenation has been shown to be a crucial structural determinant for the potency of a phenolic compound to positively modulate glycine receptor function.The aim of this in vitro study was to characterize the effects of 4-chloropropofol (4-chloro-2,6-dimethylphenol) at four glycine receptor mutations.
methodsGlycine receptor subunits were expressed in HEK 293 cells and experiments were performed using the whole-cell patch-clamp technique.
results4-chloropropofol exerted a positive allosteric modulatory effect in a low sub-nanomolar concentration range at the wild type receptor (EC50 value of 0.08 ± 0.02 nM) and in a micromolar concentration range at the mutations (1.3 ± 0.6 μM, 0.1 ± 0.2 μM, 6.0 ± 2.3 μM and 55 ± 28 μM for R271Q, L, K and S267I, respectively).
conclusions4-chloropropofol might be an effective compound for the activation of mutated glycine receptors in experimental models of startle disease.
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