Impact of intermittent voluntary ethanol consumption during adolescence on the expression of endocannabinoid system and neuroinflammatory mediators.
Alcohol Drinking
/ adverse effects
Animals
Anxiety
/ psychology
Central Nervous System Depressants
/ adverse effects
Emotions
Endocannabinoids
/ genetics
Ethanol
/ adverse effects
Gene Expression
/ drug effects
Inflammation Mediators
/ metabolism
Male
Memory
/ drug effects
Motor Activity
/ drug effects
Psychology, Adolescent
Psychomotor Performance
/ drug effects
RNA, Messenger
/ biosynthesis
Rats
Rats, Wistar
Receptors, Neuropeptide Y
/ drug effects
Anxiety
Endocannabinoid system
Neuroinflammation
Rats
Voluntary exposure
Journal
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
ISSN: 1873-7862
Titre abrégé: Eur Neuropsychopharmacol
Pays: Netherlands
ID NLM: 9111390
Informations de publication
Date de publication:
04 2020
04 2020
Historique:
received:
08
07
2019
revised:
09
01
2020
accepted:
22
01
2020
pubmed:
15
2
2020
medline:
11
8
2021
entrez:
15
2
2020
Statut:
ppublish
Résumé
The adolescent brain displays high vulnerability to the deleterious effects of ethanol, including greater risk of developing alcohol use disorder later in life. Here, we characterized the gene expression of the endocannabinoid system (ECS) and relevant signaling systems associated with neuroinflammation and emotional behaviors in the brain of young adult control and ethanol-exposed (EtOH) rats. We measured mRNA levels of candidate genes using quantitative real time PCR in the medial prefrontal cortex (mPFC), amygdala and hippocampus. EtOH rats were generated by maintenance on an intermittent and voluntary ethanol consumption during adolescence using the two-bottle choice paradigm (4 days/week for 4 weeks) followed by 2 week-withdrawal, a time-point of withdrawal with no physical symptoms. Mean differences and effect sizes were calculated using t-test and Cohen's d values. In the mPFC and hippocampus, EtOH rats had significantly higher mRNA expression of endocannabinoid-signaling (mPFC: Ppara, Dagla, Daglb and Napepld; and hippocampus: Cnr2, Dagla and Mgll) and neuroinflammation-associated genes (mPFC: Gfap; and hippocampus: Aif1) than in controls. Moreover, EtOH rats had significantly higher mRNA expression of neuropeptide Y receptor genes (Npy1r, Npy2r and Npy5r) in the hippocampus. Finally, EtOH rats also displayed higher plasma endocannabinoid levels than controls. In conclusion, these results suggest that adolescent ethanol exposure can lead to long-term alterations in the gene expression of the ECS and other signaling systems involved in neuroinflammation and regulation of emotional behaviors in key brain areas for the development of addiction.
Identifiants
pubmed: 32057593
pii: S0924-977X(20)30035-3
doi: 10.1016/j.euroneuro.2020.01.012
pii:
doi:
Substances chimiques
Central Nervous System Depressants
0
Endocannabinoids
0
Inflammation Mediators
0
RNA, Messenger
0
Receptors, Neuropeptide Y
0
Ethanol
3K9958V90M
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
126-138Informations de copyright
Copyright © 2020. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Conflict of interest None.