The primary objective of the present thesis was to examine the contribution of acetaldehyde, as well as GABA receptor agonists and glutamate receptor antagonists in mediating the discriminative stimulus effects of ethanol using a discriminative taste aversion (DTA) procedure. The DTA procedure trained animals to associate the stimulus effects of ethanol or acetaldehyde with either a saccharin-LiCl or a saccharin-saline pairing. Animals in the LiCl group learned to decrease their saccharin intake following ethanol or acetaldehyde injections but not after saline injections. Animals in the Saline groups did not decrease their saccharin intake when injected with either the training drug or saline. Experiment 1 a showed that acetaldehyde partially substituted for ethanol while experiment 1b showed that ethanol partially substituted for acetaldehyde. Administration of the catalase inhibitor aminotriazole failed to block the discriminative cue of ethanol. Animals in experiment 2 and 3 were trained to discriminate ethanol from saline. Generalization tests showed that administration of the gamma-aminotransaminase inhibitor AOAA, the GABA A agonists THIP and pentobarbital, the GABA B agonist baclofen failed to substitute for ethanol while the GABA A antagonist picrotoxin failed to block the ethanol cue. Experiment 3 showed that the NMDA antagonists MK-801 and memantine substituted for ethanol while the AMPA antagonist GYKI 52466 did not, suggesting that inhibition of the NMDA receptor, but not the AMPA receptor contributes to the stimulus effects of ethanol. Overall, the findings from the present thesis showed that the DTA procedure could quickly and reliably train animals to discriminate ethanol, and acetaldehyde, from saline. Generalization tests demonstrated that acetaldehyde and the NMDA receptor, but not the GABA A receptor, contributes to the stimulus effects of ethanol
