ArticleAlcoholism, clinical and experimental research2018
Neuroactive Steroid (3α,5α)3-hydroxypregnan-20-one (3α,5α-THP) and Pro-inflammatory Cytokine MCP-1 Levels in Hippocampus CA1 are Correlated with Voluntary Ethanol Consumption in Cynomolgus Monkey.
Article in Alcoholism, clinical and experimental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Effect of progesterone administration in male and female smokers on nicotine withdrawal and neural response to smoking cues: role of progesterone conversion to allopregnanolone.Biology of sex differences · 2022Trial
- Effects of ibudilast on central and peripheral markers of inflammation in alcohol use disorder: A randomized clinical trial.Addiction biology · 2022Trial
- Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice.International journal of molecular sciences · 2024Article
- Cholinergic and Neuroimmune Signaling Interact to Impact Adult Hippocampal Neurogenesis and Alcohol Pathology Across Development.Frontiers in pharmacology · 2022Review
- Immune treatments for alcohol use disorder: A translational framework.Brain, behavior, and immunity · 2021Review
- A Rationale for Allopregnanolone Treatment of Alcohol Use Disorders: Basic and Clinical Studies.Alcoholism, clinical and experimental research · 2020Review
- Neuroimmune signaling in alcohol use disorder.Pharmacology, biochemistry, and behavior · 2019Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNeuroactive steroids such as (3α,5α)3-hydroxypregnan-20-one (3α,5α-THP, allopregnanolone) are potent neuromodulators that enhance GABAergic neurotransmission and produce inhibitory neurobehavioral and anti-inflammatory effects. Chronic ethanol (EtOH) consumption reduces 3α,5α-THP levels in human plasma, but has brain region- and species-specific effects on central nervous system levels of 3α,5α-THP. We explored the relationship between 3α,5α-THP levels in the hippocampus and voluntary EtOH consumption in the cynomolgus monkey following daily self-administration of EtOH for 12 months and further examined the relationship with hypothalamic-pituitary-adrenal (HPA) axis function prior to EtOH exposure. We simultaneously explored hippocampus levels of monocyte chemoattractant protein 1 (MCP-1), a pro-inflammatory cytokine that plays an important role in the neuroimmune response to EtOH, following chronic self-administration.
methodsMonkeys were subjected to scheduled induction of water and EtOH consumption (0 to 1.5 g/kg) over 4 months, followed by free access to EtOH or water for 22 h/d over 12 months. Immunohistochemistry was performed using an anti-3α,5α-THP or anti-MCP-1 antibody. Prolonged voluntary drinking resulted in individual differences in EtOH consumption that ranged from 1.2 to 4.2 g/kg/d over 12 months.
resultsProlonged EtOH consumption increased cellular 3α,5α-THP immunoreactivity by 12 ± 2% (p < 0.05) and reduced MCP-1 immunoreactivity by 23 ± 9% (p < 0.05) in the hippocampus CA1. In both cases, the effect of EtOH was most pronounced in heavy drinkers that consumed ≥3 g/kg for ≥20% of days. 3α,5α-THP immunoreactivity was positively correlated with average daily EtOH intake (Spearman r = 0.76, p < 0.05) and dexamethasone inhibition of HPA axis function (Spearman r = 0.9, p < 0.05). In contrast, MCP-1 immunoreactivity was negatively correlated with average daily EtOH intake (Spearman r = -0.78, p < 0.05) and dexamethasone suppression of HPA axis function (Spearman r = -0.76, p < 0.05). Finally, 3α,5α-THP and MCP-1 immunoreactivity were inversely correlated with each other (Spearman r = -0.68, p < 0.05).
conclusionsThese data indicate that voluntary, long-term EtOH consumption results in higher levels of 3α,5α-THP, while decreasing levels of MCP-1 in the CA1 hippocampus, and that both changes may be linked to HPA axis function and the magnitude of voluntary EtOH consumption.
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