At present, little is known about the mechanisms underlying EtOH potentiation of GABA release. The increase in mIPSC frequency suggests that the site of EtOH action is downstream of action potential generation and calcium entry into the presynaptic terminal. Experiments in the cerebellum and VTA suggest that EtOH interacts with mechanisms involved in intracellular calcium release, perhaps increasing calcium concentrations in the presynaptic terminal (Kelm et al. 2007; Theile et al. 2009). It would be helpful to know whether EtOH increases calcium concentrations in the relevant population of GABAergic presynaptic terminals. However, this is difficult to determine given the small size (<1 µM diameter) of terminals, and the diversity of subtypes of terminals found on any given neuron.
