Modulating amygdala activation to traumatic memories with a single ketamine infusion
Or Duek, Yutong Li, Ben Kelmendi, Shelley Amen, Charles Gordon, Madison Milne, John H. Krystal, Ifat Levy, Ilan Harpaz-Rotem
medRxiv Preprint Server July 7, 2021 preprint DOI: 10.1101/2021.07.07.21260166 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial |
|---|---|
| Population | Humans with PTSD |
| Interventions | Ketamine Midazolam |
| Dose | single subanesthetic intravenous infusion |
| Duration | 30 days post-extinction |
| Topics | Esketamine Ketamine |
| Keywords | Trauma memory alteration Ketamine intervention Memory reconsolidation |
| Citations | 8 |
| Key findings | Ketamine given after trauma memory retrieval reduces amygdala and hippocampus reactivity to those memories for at least 30 days. |
Abstract
NMDA receptor antagonists have a vital role in extinction, learning, and reconsolidation processes. During the reconsolidation window, memories are activated into a labile state and can be stored in an altered form. This concept might have significant clinical implications in treating PTSD. Using amygdala activity as a major biomarker of fear response, we tested the potential of a single subanesthetic intravenous infusion of ketamine (NMDA receptor antagonist) to enhance post-retrieval extinction of PTSD trauma memories. Post-extinction, ketamine recipients (vs midazolam) showed a lower amygdala and hippocampus reactivation to trauma memories. Post-retrieval ketamine administration was also associated with decreased connectivity between the amygdala and hippocampus, with no change in amygdala-vmPFC connectivity, which suggests that ketamine may enhance post-retrieval extinction of PTSD trauma memory in humans. These findings demonstrate the capacity to rewrite human traumatic memories and to modulate the fear response for at least 30 days post-extinction.