Reconsolidation of appetitive memories for both natural and drug reinforcement is dependent on {beta}-adrenergic receptors.
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.
Milton
Amy L
AL
Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology, University of Cambridge, Downing Site, Cambridge CB2 3EB, United Kingdom. alm46@cam.ac.uk
Lee
Jonathan L C
JL
Everitt
Barry J
BJ
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003042:Cocaine / Q000008:administration & dosage; D003214:Conditioning, Classical / Q000187:drug effects / Q000502:physiology*; D005108:Extinction, Psychological; D008297:Male; D008568:Memory / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D012054:Reinforcement, Psychology; D012646:Self Administration; D015398:Signal Transduction / Q000502:physiology*; D013395:Sucrose
D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D013395:Sucrose; D011433:Propranolol; D003042:Cocaine