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Amygdala dopamine receptors are required for the destabilization of a reconsolidating appetitive memory

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Version 2 2023-06-12, 09:01
Version 1 2023-06-09, 16:54
journal contribution
posted on 2023-06-12, 09:01 authored by Emiliano MerloEmiliano Merlo, Patrizia Ratano, Elena C Ilioi, Miranda A L S Robbins, Barry J Everitt, Amy L Milton
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.

History

Publication status

  • Published

File Version

  • Published version

Journal

eNeuro

ISSN

2373-2822

Publisher

Society for Neuroscience

Issue

1

Volume

2

Page range

1-14

Department affiliated with

  • Psychology Publications

Full text available

  • Yes

Peer reviewed?

  • Yes

Legacy Posted Date

2019-02-18

First Open Access (FOA) Date

2019-02-18

First Compliant Deposit (FCD) Date

2019-02-15

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