Alcohol Dependence in Rats Is Associated with Global Changes in Gene Expression in the Central Amygdala.
RNA-Seq
alcohol use disorder (AUD)
central nucleus of the amygdala (CeA)
chronic intermittent alcohol vapor
differentially expressed genes (DEGs)
extracellular matrix
Journal
Brain sciences
ISSN: 2076-3425
Titre abrégé: Brain Sci
Pays: Switzerland
ID NLM: 101598646
Informations de publication
Date de publication:
29 Aug 2021
29 Aug 2021
Historique:
received:
14
08
2020
revised:
06
08
2021
accepted:
21
08
2021
entrez:
28
9
2021
pubmed:
29
9
2021
medline:
29
9
2021
Statut:
epublish
Résumé
Alcohol dependence is associated with adverse consequences of alcohol (ethanol) use and is evident in most severe cases of alcohol use disorder (AUD). The central nucleus of the amygdala (CeA) plays a critical role in the development of alcohol dependence and escalation of alcohol consumption in dependent subjects. Molecular mechanisms underlying the CeA-driven behavioral changes are not well understood. Here, we examined the effects of alcohol on global gene expression in the CeA using a chronic intermittent ethanol (CIE) vapor model in rats and RNA sequencing (RNA-Seq). The CIE procedure resulted in robust changes in CeA gene expression during intoxication, as the number of differentially expressed genes (DEGs) was significantly greater than those expected by chance. Over-representation analysis of cell types, functional groups and molecular pathways revealed biological categories potentially important for the development of alcohol dependence in our model. Genes specific for astrocytes, myelinating oligodendrocytes, and endothelial cells were over-represented in the DEG category, suggesting that these cell types were particularly affected by the CIE procedure. The majority of the over-represented functional groups and molecular pathways were directly related to the functions of glial and endothelial cells, including extracellular matrix (ECM) organization, myelination, and the regulation of innate immune response. A coordinated regulation of several ECM metalloproteinases (e.g.,
Identifiants
pubmed: 34573170
pii: brainsci11091149
doi: 10.3390/brainsci11091149
pmc: PMC8468792
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : NIAAA NIH HHS
ID : R01 AA027700
Pays : United States
Organisme : NIAAA NIH HHS
ID : U24 AA025479
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA006420
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA024836
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA021491
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA015566
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA017447
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA027096
Pays : United States
Organisme : NIAAA NIH HHS
ID : R01 AA021491
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA013498
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA025479
Pays : United States
Organisme : NIAAA NIH HHS
ID : U01 AA013498
Pays : United States
Organisme : NIAAA NIH HHS
ID : P60 AA006420
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA017447
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA025408
Pays : United States
Organisme : NIAAA NIH HHS
ID : AA027700
Pays : United States
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