BACKGROUND: The retrieval of consolidated memories may result in their destabilization, requiring a restabilization process called reconsolidation. During reconsolidation, memories become sensitive to psychological and pharmacological modifications again, thus providing an opportunity to alter unwanted memories. Although such reconsolidation manipulations might open the door to novel treatment approaches for psychiatric disorders such as posttraumatic stress disorder, the brain mechanisms underlying reconsolidation processes in humans are completely unknown. Here, we asked whether a β-adrenergic receptor antagonist might interfere with the reconsolidation of emotional episodic memories and what brain mechanisms are involved in these effects. METHODS: Healthy participants were administered the β-adrenergic receptor antagonist propranolol or a placebo before they reactivated previously learned neutral and emotional material. Recognition memory was tested 24 hours later. Functional magnetic resonance images were collected during reactivation and recognition testing. RESULTS: Propranolol during reactivation specifically reduced the subsequent memory for emotional pictures; memory for neutral pictures remained unaffected. This emotional memory impairment was associated with significantly increased activity in the amygdala and the hippocampus for correctly recognized pictures at test. Most interestingly, the same structures were active (but not modulated by propranolol) during memory reactivation. Memory reactivation alone or propranolol without reactivation had no effect on subsequent memory. CONCLUSIONS: Our results demonstrate how the consequences of memory reconsolidation processes are represented in the human brain, suggesting that the brain areas that are recruited during reactivation undergo changes in activity that are associated with subsequent memory recall.
BACKGROUND: The retrieval of consolidated memories may result in their destabilization, requiring a restabilization process called reconsolidation. During reconsolidation, memories become sensitive to psychological and pharmacological modifications again, thus providing an opportunity to alter unwanted memories. Although such reconsolidation manipulations might open the door to novel treatment approaches for psychiatric disorders such as posttraumatic stress disorder, the brain mechanisms underlying reconsolidation processes in humans are completely unknown. Here, we asked whether a β-adrenergic receptor antagonist might interfere with the reconsolidation of emotional episodic memories and what brain mechanisms are involved in these effects. METHODS: Healthy participants were administered the β-adrenergic receptor antagonist propranolol or a placebo before they reactivated previously learned neutral and emotional material. Recognition memory was tested 24 hours later. Functional magnetic resonance images were collected during reactivation and recognition testing. RESULTS:Propranolol during reactivation specifically reduced the subsequent memory for emotional pictures; memory for neutral pictures remained unaffected. This emotional memory impairment was associated with significantly increased activity in the amygdala and the hippocampus for correctly recognized pictures at test. Most interestingly, the same structures were active (but not modulated by propranolol) during memory reactivation. Memory reactivation alone or propranolol without reactivation had no effect on subsequent memory. CONCLUSIONS: Our results demonstrate how the consequences of memory reconsolidation processes are represented in the human brain, suggesting that the brain areas that are recruited during reactivation undergo changes in activity that are associated with subsequent memory recall.