Blackout (alcohol-related Amnesia) - Neurophysiological/chemical Mechanisms

Neurophysiological/chemical Mechanisms

Memory disruptions by alcohol leading to blackout have been linked to inhibition of long-term potentiation, particularly in the hippocampus, by affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate neurotransmission (see Effects of alcohol on memory).

Alcohol induced blackouts are associated with the development of alcohol abuse and dependence, so it is important to consider potential neurobiological risk factors for experiencing this problem prior to onset of substance use. Results showed that prior to beginning substance use, blackout + youth showed greater activation during inhibitory processing than nondrinkers and blackout – youth in frontal and cerebellar brain regions. Activation during correct inhibitory responses relative to go responses in the left and middle frontal gyri at baseline predicted future blackout experience, after controlling for follow-up externalizing behaviors and lifetime alcohol consumption. The conclusion of this study was that substance-naïve adolescents who later experience alcohol-induced blackouts show increased neural effort during inhibitory processing, as compared to adolescents who go on to drink at similar levels, but do not experience blackouts and healthy, nondrinking controls, suggesting a neurobiological vulnerability to alcohol-induced memory impairments.