Mixed results with the synthetic β-adrenergic receptor blocker, propranolol, have been reported in human populations with regards to its therapeutic efficacy for PTSD treatments targeting the memory reconsolidation process. Stress alters the ability to form and maintain memory, but whether the causal neuronal mechanisms underling memory formation in PTSD are similar to normal memory is not clear. Here, we use Lymnaea to study the effects of combinations of stressors on the quality of the formed memory state. We show reactivation dependent pharmacologic disruption of reconsolidation using propranolol in Lymnaea; specifically, we show that only certain memories created under conditions of a combination of stressors are susceptible to disruption. Our data suggest that phenotypically similar memories may be molecularly diverse, depending on the conditions under which they are formed. Applied to human PTSD, this could account for the mixed results in the literature on disrupting reconsolidation with propranolol.
Keywords: Long-term memory; Lymnaea; Propranolol; Reconsolidation.
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