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Etifoxine: Difference between revisions
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[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364751/pdf/pone.0120473.pdf do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473] | [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364751/pdf/pone.0120473.pdf do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473] | ||
etifoxine therapy promoted the regeneration of axons | |||
<ref>[http://www.pnas.org/content/105/51/20505.full.pdf Etifoxine improves peripheral nerve regeneration and functional recovery]</ref> | |||
<references/> | <references/> | ||
Revision as of 19:06, 5 August 2016
etifoxine is an anticonvulsant and ansiolytic agent. It is not recommended under the age of 18 years.[1]
The known mechanism oof action is potentiation of GABAA receptor, via stimulation of neurosteroid production. [2]
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Etifoxine promotes glial‑derived neurotrophic factor‑induced neurite outgrowth in PC12 cells
do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473 etifoxine therapy promoted the regeneration of axons [3]