Glucocorticoid receptor antagonism disrupts the reconsolidation of social reward-related memories in rats.
Reconsolidation is the process whereby consolidated memories are destabilized upon retrieval and restabilized to persist for later use. Although the neurobiology of the reconsolidation of both appetitive and aversive memories has been intensively investigated, reconsolidation of memories of physiologically relevant social rewards has received little attention. Social play, the most characteristic social behaviour displayed by young mammals, is highly rewarding, illustrated by the fact that it can induce conditioned place preference (CPP). Here, we investigated the role of signalling mechanisms implicated in memory processes, including reconsolidation, namely glucocorticoid, mineralocorticoid, NMDA glutamatergic and CB1 cannabinoid receptors, in the reconsolidation of social play-induced CPP in rats. Systemic treatment with the glucocorticoid receptor antagonist mifepristone before, but not immediately after, retrieval disrupted the reconsolidation of social play-induced CPP. Mifepristone did not affect social play-induced CPP in the absence of memory retrieval. Treatment with the NMDA receptor antagonist MK-801 modestly affected the reconsolidation of social play-induced CPP. However, the reconsolidation of social play-induced CPP was not affected by treatment with the mineralocorticoid and CB1 cannabinoid receptor antagonists spironolactone and rimonabant, respectively. We conclude that glucocorticoid neurotransmission mediates the reconsolidation of social reward-related memories in rats. These data indicate that the neural mechanisms of the reconsolidation of social reward-related memories only partially overlap with those underlying the reconsolidation of other reward-related memories.
aDepartment of Animals in Science and Society, Division of Behavioural Neuroscience, Faculty of Veterinary Medicine, Utrecht University bDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands cDepartment of Science, Section of Biomedical Sciences and Technologies, University 'Roma Tre', Rome, Italy.
E J Marijke
EJ
Achterberg
Viviana
V
Trezza
Louk J M J
LJ
Vanderschuren
D000704:Analysis of Variance; D000818:Animals; D063387:Cannabinoid Receptor Antagonists / Q000494:pharmacology; D003216:Conditioning, Operant / Q000187:drug effects*; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006727:Hormone Antagonists / Q000633:toxicity*; D008297:Male; D008569:Memory Disorders / Q000139:chemically induced*; D015735:Mifepristone / Q000633:toxicity*; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D018696:Neuroprotective Agents / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012201:Reward; D000077285:Rimonabant; D012919:Social Behavior; D013148:Spironolactone / Q000494:pharmacology
D063387:Cannabinoid Receptor Antagonists; D006727:Hormone Antagonists; D000451:Mineralocorticoid Receptor Antagonists; D018696:Neuroprotective Agents; D010880:Piperidines; D011720:Pyrazoles; D013148:Spironolactone; D015735:Mifepristone; D016291:Dizocilpine Maleate; D000077285:Rimonabant