Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by activating β2 and β3 subunit containing channels of the GABA A receptor complex (a different binding site than benzodiazepines), and by stimulating the production of GABA(A) active neurosteroids that act in conjunction with etifoxine's direct effects.  This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites;  however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil . 
Thiamin (B1) deficiency results in a loss of thiamin-containing nerve endings, changing the balance of neurotransmitters in the brain including GABA. 30-32 Manganese is also essential to the synthesis of glutamine. Glutamine, in turn, is essential for the synthesis of niacin (B3.) GABA is involved in glucose metabolism 36 as well as that of vitamin C. 33,34 Lysine enhances GABA's action in the brain, while aspartate inhibits glutamic acid. A number of food additives inhibit GABA receptors, while many perfumes enhance their responsiveness. 35 Taurine, another amino acid, helps break glutamate down to GABA, and it too seems to act as a CNS sedative.