RT Journal Article
SR Electronic
T1 Amygdala Dopamine Receptors Are Required for the Destabilization of a Reconsolidating Appetitive Memory
JF eneuro
JO eneuro
FD Society for Neuroscience
SP ENEURO.0024-14.2015
DO 10.1523/ENEURO.0024-14.2015
VO 2
IS 1
A1 Emiliano Merlo
A1 Patrizia Ratano
A1 Elena C. Ilioi
A1 Miranda A.L.S. Robbins
A1 Barry J. Everitt
A1 Amy L. Milton
YR 2015
UL http://www.eneuro.org/content/2/1/ENEURO.0024-14.2015.abstract
AB 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.