The Acute Effects of Psychoactive Drugs on Emotional Episodic Memory Encoding, Consolidation, and Retrieval
Study at a glance
AI-extracted from the abstract| Characteristics | Review |
|---|---|
| Interventions | Alcohol Benzodiazepines Ketamine Dopaminergic/noradrenergic stimulants MDMA Dextroamphetamine |
| Key findings | The authors argue that psychoactive drugs modulate emotional episodic memory in stage- and drug-specific ways: pre-encoding GABAA sedatives, THC, and ketamine preferentially impair emotional memories, stimulants enhance them, and MDMA does both; post-encoding GABAA sedatives enhance emotional memories with specificity declining as encoding-to-retrieval delay increases; and retrieval under THC, dextroamphetamine, or MDMA increases false memories, with some evidence of preferential distortion of emotional, especially positive, memories. |
Abstract
Psychoactive drugs modulate learning and emotional processes in ways that could impact their recreational and medical use. Recent work has revealed how drugs impact different stages of processing emotional episodic memories, including encoding (formation of memory traces), consolidation (stabilization of memory traces), and retrieval (accessing memory traces). Drugs administered before encoding more selectively modulate emotional (negative and/or positive) vs. neutral memories with preferential impairments (e.g., GABAA sedatives like alcohol and benzodiazepines, Δ9-tetrahydrocannabinol or THC, ketamine), enhancements (e.g., dopaminergic/noradrenergic stimulants), or both preferential impairments and enhancements (i.e., ±3,4-methylenedioxymethylamphetamine or MDMA) of emotional memories. GABAA sedatives administered immediately post-encoding (during consolidation) preferentially enhance emotional memories, and the specificity of this effect declines as the delay between encoding and retrieval increases. Finally, retrieving memories under the effects of THC, dextroamphetamine, and MDMA increases false memories, with some evidence for preferential distortions of emotional (especially positive) memories. We propose neural mechanisms underlying these effects, methodological considerations for future work, and how drug effects on emotional episodic memory may contribute to drug use and abuse.