Modulation of object memory consolidation by heroin and heroin-conditioned stimuli: Role of opioid and noradrenergic systems

There is recent evidence that cocaine, nicotine, and their conditioned stimuli have the ability to enhance memory consolidation. The present study compared the effects of post-training heroin and of a heroin contextual conditioned stimulus (CS+) on consolidation of object recognition memory and inve...

Full description

Saved in:
Bibliographic Details
Published inEuropean neuropsychopharmacology Vol. 33; pp. 146 - 157
Main Authors Wolter, Michael, Huff, Andrew E., Baidoo, Nana, Jardine, Kristen H., Pulles, Zoey, Winters, Boyer D., Leri, Francesco
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.04.2020
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:There is recent evidence that cocaine, nicotine, and their conditioned stimuli have the ability to enhance memory consolidation. The present study compared the effects of post-training heroin and of a heroin contextual conditioned stimulus (CS+) on consolidation of object recognition memory and investigated the roles of opioid and beta-adrenergic receptors in heroin/CS+ memory modulation by co-administering the respective antagonists, naltrexone (NTX) and propranolol (PRO). Three experiments were performed in male Sprague-Dawley rats demonstrating that immediate, but not delayed, post-sample exposure to heroin (0.3, 1 mg/kg), or exposure (30 min) to a contextual CS+ paired with 1 mg/kg heroin (5 pairings, each 120 min), equally enhanced object memory. Importantly, while the memory enhancing effects of 1 mg/kg heroin and of the contextual CS+ were not altered by post-training co-administration of 3 mg/kg naltrexone, they were blocked by post-training co-administration of 10 mg/kg propranolol. Taken together, these data suggest that a context paired with heroin shares the memory enhancing effect of heroin itself and that these unconditioned and conditioned drug stimuli may modulate memory through the activation of beta-noradrenergic receptors.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0924-977X
1873-7862
DOI:10.1016/j.euroneuro.2020.01.010