Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on B-adrenergic receptors
Research output: Contribution to journal › Article
Colleges, School and Institutes
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.
|Number of pages||5|
|Journal||Learning & memory|
|Publication status||Published - 1 Jan 2008|