mechanism is unlikely to explain the acute differences observed in the current study. Increased GABA release also occurs in response to ethanol administration and is induced, at least in part, by a presynaptic GABAA receptor mechanism [35], [36]. The α2-subunit has been found presynaptically in hippocampal mossy fibre neurons [37] and thus may serve to modulate GABA release. Since presynaptic GABA receptors attenuate ethanol-induced GABA release [36], it might be speculated that a deletion of the α2-subunit would result in increased GABA release in response to an ethanol challenge, causing an enhanced acute response. However, it is important to note that evidence of presynaptically expressed α2-subunits in brain regions other than hippocampus, and a direct link with ethanol effects remains to be demonstrated.
