GlyT-2 mediates the forskolin-induced increase of glycinergic transmission

In this study, we have examined the possible roles of a glycine transporter type 2 (GlyT-2) in the forskolin-induced increase of the amplitude of glycinergic miniature inhibitory postsynaptic currents (mIPSCs) in acutely isolated rat substantia gelatinosa neurons. Forskolin, an adenylyl cyclase activator, increased the amplitude of glycinergic mIPSCs in the presence, but not in the absence, of a low concentration of extracellular glycine. This effect disappeared by the addition of ALX1393 (a GlyT-2 antagonist). These results suggest that both extracellular glycine and GlyT-2 are essential for the forskolin-induced increase in the amplitude of glycinergic mIPSCs. These mechanisms might contribute, at least in part, to the maturation of inhibitory synaptic transmission, including the developmental neurotransmitter switch from GABA to glycine within the spinal dorsal horn during postnatal development.