Glutamatergic neurons in the medial prefrontal cortex mediate the formation and retrieval of cocaine-associated memories in mice.
Animals
Cocaine
/ pharmacology
Cocaine-Related Disorders
/ physiopathology
Disease Models, Animal
Dopamine Uptake Inhibitors
/ pharmacology
Electrophysiology
Fluorescent Antibody Technique
GABAergic Neurons
/ drug effects
Male
Memory
/ drug effects
Mice
Mice, Inbred C57BL
Prefrontal Cortex
/ drug effects
DREADD
addiction
cocaine
glutamate
medial prefrontal cortex
memory
Journal
Addiction biology
ISSN: 1369-1600
Titre abrégé: Addict Biol
Pays: United States
ID NLM: 9604935
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
17
07
2018
revised:
04
12
2018
accepted:
10
01
2019
pubmed:
9
2
2019
medline:
11
2
2021
entrez:
9
2
2019
Statut:
ppublish
Résumé
In drug addiction, environmental stimuli previously associated with cocaine use readily elicit cocaine-associated memories, which persist long after abstinence and trigger cocaine craving and consumption. Although previous studies suggest that the medial prefrontal cortex (mPFC) is involved in the expression of cocaine-addictive behaviors, it remains unclear whether excitatory and inhibitory neurons in the mPFC are causally related to the formation and retrieval of cocaine-associated memories. To address this issue, we used the designer receptors exclusively activated by designer drugs (DREADD) technology combined with a cocaine-induced conditioned place preference (CPP) paradigm. We suppressed mPFC neuronal activity in a cell-type- and timing-dependent manner. C57BL/6J wild-type mice received bilateral intra-mPFC infusion of an adeno-associated virus (AAV) expressing inhibitory DREADD (hM4Di) under the control of CaMKII promotor to selectively suppress mPFC pyramidal neurons. GAD67-Cre mice received bilateral intra-mPFC infusion of a Cre-dependent AAV expressing hM4Di to specifically silence GABAergic neurons. Chemogenetic suppression of mPFC pyramidal neurons significantly attenuated both the acquisition and expression of cocaine CPP, while suppression of mPFC GABAergic neurons affected neither the acquisition nor expression of cocaine CPP. Moreover, chemogenetic inhibition of mPFC glutamatergic neurons did not affect the acquisition and expression of lithium chloride-induced conditioned place aversion. These results suggest that the activation of glutamatergic, but not GABAergic, neurons in the mPFC mediates both the formation and retrieval of cocaine-associated memories.
Substances chimiques
Dopamine Uptake Inhibitors
0
Cocaine
I5Y540LHVR
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12723Subventions
Organisme : Grant-in-Aid for Scientific Research (B) from the Japan Society for the Promotion of Science
ID : 18H02523
Pays : International
Organisme : Grant-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science
ID : 15K06765
Pays : International
Organisme : Grant-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science
ID : 18K06520
Pays : International
Organisme : The Naito Foundation (K.K.)
Pays : International
Organisme : Smoking Research Foundation (K.K.)
Pays : International
Organisme : Hoansha Foundation (K.K.)
Pays : International
Informations de copyright
© 2019 Society for the Study of Addiction.
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