Proton receptors regulate synapse-specific reconsolidation in the amygdala

Abstract

When an extinction procedure is performed within the reconsolidation window, the original aversive memory can be replaced by one that is less traumatic. Recent studies revealed that carbon dioxide (CO2) inhalation during retrieval enhances memory lability. However, the effects of CO2 inhalation on the central nervous system can be extensive, and there is lack of evidence suggesting that the effects of CO2 are selective to a reactivated memory. We discovered that CO2 inhalation paired with memory retrieval potentiates the specific aversive memory trace, resulting in greater memory lability. The specific effects of CO2 depend on acid-sensing ion channels (ASICs), the proton receptors that are involved in synaptic transmission and plasticity in the amygdala. In addition, CO2 inhalation alters memory lability via synaptic plasticity at selectively targeted synapses. Overall, our results suggest that inhaling CO2 during the retrieval event increases the lability of an aversive memory through a synapse-specific reconsolidation process.