Étifoxine et récepteurs GABA

The currents induced by GABA in neuronal cultures are potentiated by etifoxine, even in the presence of a benzodiazepine site antagonist, thus confirming that etifoxine does not bind to this site. Other studies of recombinant receptors show that the potentiation persists in the absence of α or γ subunits, which suggests that the β subunit plays a major role in the effects of etifoxine. This is confirmed by the fact that the degree of potentiation depends on the nature of the β subunit co-expressed with α and β ; the potentiation obtained is in fact markedly more pronounced for receptors containing a β2 or β3 than for those containing a β1 subunit. This preference for β2 and β3 distinguishes etifoxine from other positive GABAA receptor modulators such as neurosteroids or benzodiazepines, the modulatory effects of which are relatively unaffected by the nature of the β subunit. The specificity of the mechanism of action of etifoxine on GABAA receptors might contribute to its original therapeutic properties.