As anyone who's ever taken an Alcohol Edu course (or been 21 in the last decade) knows, consuming too much alcohol can cause memory loss, colloquially known as a "blackout". This anterograde amnesia stems from an inability of the brain to form new long-term memories and is caused by a disruption in the GABA and NMDA receptors in the prefrontal cortex (PFC) and medial temporal lobes when drinking.
First, for those of you who skipped (or drank) your way through your alcohol education, a brief reminder on the effects of alcohol on the brain. GABA is a primary inhibitory neurotransmitter, acting to decrease the likelihood of a cell's firing. Alcohol acts as a GABA agonist, elevating levels throughout the brain and therefore diminishing the rates of firing in normal cellular processes. At high levels, alcohol also acts upon glutamate NMDA receptors, one of the main excitatory neurotransmitter systems. Alcohol works as an NMDA antagonist, blocking the NMDA receptors and preventing glutamatergic activation, further inhibiting neuronal functioning. This inhibition particularly occurs in the PFC, medial temporal cortex and the parietal lobe, primary targets of alcohol in the brain. In the hippocampus in particular, an area in the medial temporal cortex crucial to memory formation, this inhibition can result in a disruption of long-term potentiation, a cellular process involved in the consolidation of short-term to long-term memories.