Abstract
Disrupting maladaptive memories may provide a novel form of treatment for neuropsychiatric disorders, but little is known about the neurochemical mechanisms underlying the induction of lability, or destabilization, of a retrieved consolidated memory. Destabilization has been theoretically linked to the violation of expectations during memory retrieval, which, in turn, has been suggested to correlate with prediction error (PE). It is well-established that PE correlates with dopaminergic signaling in limbic forebrain structures that are critical for emotional learning. The basolateral amygdala is a key neural substrate for the reconsolidation of pavlovian reward-related memories, but the involvement of dopaminergic mechanisms in inducing lability of amygdala-dependent memories has not been investigated. Therefore, we tested the hypothesis that dopaminergic signaling within the basolateral amygdala is required for the destabilization of appetitive pavlovian memories by investigating the effects dopaminergic and protein synthesis manipulations on appetitive memory reconsolidation in rats. Intra-amygdala administration of either the D1-selective dopamine receptor antagonist SCH23390 or the D2-selective dopamine receptor antagonist raclopride prevented memory destabilization at retrieval, thereby protecting the memory from the effects of an amnestic agent, the protein synthesis inhibitor anisomycin. These data show that dopaminergic transmission within the basolateral amygdala is required for memory labilization during appetitive memory reconsolidation.
Highlights
Reconsolidation is the process by which memories become destabilized at retrieval and subsequently restabilize in order to persist in the brain
Due to a non-normal distribution, instrumental training data were transformed prior to analysis, and analysis of these transformed data revealed that instrumental responding increased across the training sessions (Session: F(6.1,421) ϭ 13.0, p Ͻ 0.001, 2 ϭ 0.16), though with no differences in instrumental responding between the prospective experimental groups assigned to receive dopamine receptor antagonists or vehicle prior to reactivation (Drug1) and anisomycin or vehicle after reactivation (Drug2) (Session ϫ Drug1: F(18,421) ϭ 1.59, p ϭ 0.058; Session ϫ Drug2: F(6.1,421) ϭ 1.25, p ϭ 0.28; Session ϫ Drug1 ϫ Drug2: F Ͻ 1; Drug1: F Ͻ 1; Drug2: F Ͻ 1; Drug1 ϫ Drug2: F Ͻ 1)
The data presented here demonstrate that blocking dopaminergic signaling within the basolateral amygdala (BLA) either at the D1 receptor (D1R) with SCH23390 or at the D2R with raclopride prevented the amnesia that normally follows post-reactivation protein synthesis inhibition
Summary
Reconsolidation is the process by which memories become destabilized at retrieval and subsequently restabilize in order to persist in the brain. This process has received much interest for its potential as a novel treatment target for neuropsychiatric disorders such as drug addiction (Milton and Everitt, 2012; Tronson and Taylor, 2013) and post-traumatic stress disorder (PTSD; Debiec and LeDoux, 2006). Understanding the specific mechanisms that underlie memory destabilization is important from both basic science and translational perspectives
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