Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on β-adrenergic receptors

We have investigated the neurochemical mechanisms of memory reconsolidation and, in particular, the functional requirement for intracellular mechanisms initiated by β-adrenergic signaling. We show that propranolol, given in conjunction with a memory reactivation session, can specifically disrupt the...

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Bibliographic Details
Published inLearning & memory (Cold Spring Harbor, N.Y.) Vol. 15; no. 2; pp. 88 - 92
Main Authors Milton, Amy L., Lee, Jonathan L.C., Everitt, Barry J.
Format Journal Article
LanguageEnglish
Published 01.02.2008
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Summary:We have investigated the neurochemical mechanisms of memory reconsolidation and, in particular, the functional requirement for intracellular mechanisms initiated by β-adrenergic signaling. We show that propranolol, given in conjunction with a memory reactivation session, can specifically disrupt the conditioned reinforcing properties of a previously appetitively reinforced conditioned stimulus (CS), whether the stimulus had been associated with self-administered cocaine or with sucrose. These data show that memories for both drug and nondrug CS–US associations are dependent on β-adrenergic receptor-mediated signaling for their reconsolidation, with implications for the potential development of a novel treatment for drug addiction and some forms of obesity.
ISSN:1072-0502
1549-5485
DOI:10.1101/lm.825008