4.3 Article

Repetitive binge-like consumption based on the Drinking-in-the-Dark model alters the microglial population in the mouse hippocampus

Journal

JOURNAL OF INTEGRATIVE NEUROSCIENCE
Volume 20, Issue 4, Pages 933-943

Publisher

IMR PRESS
DOI: 10.31083/j.jin2004094

Keywords

Alcohol use disorder; Microglia; Neuroimmune; Amygdala; Hippocampus; Binge-like drinking

Categories

Funding

  1. High Point University, National Institute on Alcohol Abuse and Alcoholism [U54AA019765, U01 AA019925-11]
  2. National Institute of General Medical Sciences [SC1GM139696]
  3. US Department of Education

Ask authors/readers for more resources

Alcoholism leads to maladaptations in the central nervous system, including the neuroimmune system. Research on binge-like alcohol consumption shows changes in microglial reactivity, particularly in the hippocampus, indicating a potential role in the development of alcohol use disorders. Ethanol-induced upregulation of microglial genes suggests a persistent altered neuroimmune state even after periods of abstinence.
Alcoholism causes various maladaptations in the central nervous system, including the neuroimmune system. Studies of alcohol induced dysregulation of the neuroimmune system generally focus on alcohol dependence and brain damage, but our previous research indicates that repetitive binge-like consumption perturbs cytokines independent of cell death. This paper extends that research by examining the impact of binge-like consumption on microglia in the hippocampus and the amygdala. Microglia were assessed using immunohistochemistry following binge-like ethanol consumption based on Drinking-in-the-Dark model. Immunohistochemistry results showed that binge-like ethanol consumption caused an increase in Iba-1 immunoreactivity and the number of Iba-1+ cells after one Drinking-in-the-Dark cycle. However, after three Drinking-in the-Dark cycles, the number of microglia decreased in the hippocampus. We showed that in the dentate gyrus, the average immunoreactivity/cell was increased following ethanol exposure despite the decrease in number after three cycles. Likewise, Ox-42, an indicator of microglia activation, was upregulated after ethanol consumption. No significant effects on microglia number or immunoreactivity (Iba-1 nor Ox-42) were observed in the amygdala. Finally, ethanol caused an increase in the expression of the microglial gene Aif-1 during intoxication and ten days into abstinence, suggesting persistence of ethanol-induced upregulation of microglial genes. Altogether, these findings indicate that repetitive binge-like ethanol is sufficient to elicit changes in microglial reactivity. This altered neuroimmune state may contribute to the development of alcohol use disorders.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.3
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available