Journal
LEARNING & MEMORY
Volume 15, Issue 2, Pages 88-92Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/lm.825008
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Funding
- MRC [G0600196] Funding Source: UKRI
- Medical Research Council [G0600196, G0001354] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [G0001354, G0001354B, G0600196] Funding Source: researchfish
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We have investigated the neurochemical mechanisms of memory reconsolidation and, in particular, the functional requirement for intracellular mechanisms initiated by beta-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 beta-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.
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