Figure 3. Schematic model of ethanol-induced state-dependent memory. Ethanol activates GABAA receptors which conduct Cl-, resulting in neuronal hyperpolarization. Furthermore, PKC has a modulatory effect in the response of the GABAA receptor to ethanol. Also, ethanol influences NMDA receptors which lead to inhibition of EPSP which decreased LTP. It is possible that ethanol causes storage deficiency in the training day and does not affect retrieval in the testing day hence producing a state-dependent memory (Miller et al., 1978).
