GABA and glycine compete for uptake into synaptic vesicles by a shared vesicular inhibitory amino acid transporter called VIAAT or vGAT.

The present dogma states that GABA and glycine are released from single synaptic vesicles in direct proportion to their concentration in the presynaptic cytosol.

This review examines the experimental evidence concerning GABA/glycine accumulation into synaptic vesicles.

Together, the data implies that the GABA/glycine content of vesicles may be carefully regulated, perhaps at the level of each presynaptic terminal.

Changes in vesicle content at inhibitory terminals may be a form of medium-term presynaptic plasticity.