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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Published in | Learning & memory (Cold Spring Harbor, N.Y.) Vol. 15; no. 2; pp. 88 - 92 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
01.02.2008
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Online Access | Get full text |
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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. |
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ISSN: | 1072-0502 1549-5485 |
DOI: | 10.1101/lm.825008 |