It has been recently hypothesized that Schwann cells in the peripheral nervous system (PNS) are targets for GABA's action, as shown by the presence of GABA-A and GABA-B receptors. Schwann cells respond to a variety of GABAergic ligands, including neuroactive steroids. Allopregnanolone (ALLO), a reduced metabolite of progesterone, modulates allosterically the GABA-A receptor in Schwann cells and increases mRNA and protein levels of PMP22, an important myelin protein of the PNS. This observation is supported by the evidence that muscimol (GABA-A agonist) similarly enhances PMP22 mRNA levels, whereas bicuculline (GABA-A antagonist) counteracts such increase. The expression of PMP22 in Schwann cells, therefore, seems to be under the control of GABA-A receptors. Consequently, we aimed at elucidating ALLO's-mediated mechanism(s) in Schwann cells, and its putative effects on GABA synthesis. We demonstrated the presence of glutamic acid decarboxylase of 67 kDa (GAD67), an enzyme deputed to GABA synthesis, as well as the direct synthesis of GABA in Schwann cells. Additionally, we showed that ALLO enhances the GAD67 levels in Schwann cells, suggesting that PKA pathway is the intracellular signalling pathway responsible for such an allosteric action of ALLO at GABA-A receptor. These mechanisms might be of great interest to establish new strategies to treat peripheral neuropathies.