ArticleAlcoholism, clinical and experimental research2018
Acute Ethanol Inhibition of Adult Hippocampal Neurogenesis Involves CB1 Cannabinoid Receptor Signaling.
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 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Alcohol addiction and Alzheimer's disease: a molecular collision course.Translational psychiatry · 2025Review
- Cannabinoids and alcohol co-exposure modulate pathogen-induced pulmonary immune responses.Frontiers in immunology · 2025Article
- Alcohol activates cannabinoid receptor 1 and 2 in a model of pathogen induced pulmonary inflammation.Toxicology letters · 2024Article
- Alcohol-Endocannabinoid Interactions: Implications for Addiction-Related Behavioral Processes.Alcohol research : current reviews · 2022Review
- Recovery of Hippocampal-Dependent Learning Despite Blunting Reactive Adult Neurogenesis After Alcohol Dependence.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Differential expression of microRNAs in the hippocampi of male and female rodents after chronic alcohol administration.Biology of sex differences · 2020Article
- Interactions Between Alcohol and the Endocannabinoid System.Alcoholism, clinical and experimental research · 2020Review
- Cannabis and Alcohol: From Basic Science to Public Policy.Alcoholism, clinical and experimental research · 2019Article
- Changes in Neuroimmune and Neuronal Death Markers after Adolescent Alcohol Exposure in Rats are Reversed by Donepezil.Scientific reports · 2019Article
- Combined ∆Psychopharmacology · 2019Article
- Pindolol Rescues Anxiety-Like Behavior and Neurogenic Maladaptations of Long-Term Binge Alcohol Intake in Mice.Frontiers in behavioral neuroscience · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic ethanol (EtOH) exposure has been found to inhibit adult hippocampal neurogenesis in multiple models of alcohol addiction. However, acute EtOH inhibition of adult neurogenesis is not well studied. Although many abused drugs have been found to inhibit adult neurogenesis, few have studied cannabinoids or cannabinoids with EtOH, although human use of both together is becoming more common. We used an acute binge alcohol drinking model in combination with select cannabinoid receptor agonists and antagonists to investigate the actions of each alone and together on hippocampal neurogenesis.
methodsAdult male Wistar rats were treated with an acute binge dose of EtOH (5 g/kg, i.g.), cannabinoid 1 receptor (CB1R) or cannabinoid 2 receptor (CB2R) agonists, as well as selective cannabinoid (CB) antagonists, alone or combined. Hippocampal doublecortin (DCX), Ki67, and activated cleaved caspase-3 (CC3) immunohistochemistry were used to assess neurogenesis, neuroprogenitor proliferation, and cell death, respectively.
resultsWe found that treatment with EtOH or the CB1R agonist, arachidonoyl-2'-chloroethylamide (ACEA), and the combination significantly reduced DCX-positive neurons (DCX + IR) in dentate gyrus (DG) and increased CC3. Further, using an inhibitor of endocannabinoid metabolism, for example, JZL195, we also found reduced DCX + IR neurogenesis. Treatment with 2 different CB1R antagonists (AM251 or SR141716) reversed both CB1R agonist and EtOH inhibition of adult neurogenesis. CB2R agonist HU-308 treatment did not produce any significant change in DCX + IR. Interestingly, neither EtOH nor CB1R agonist produced any alteration in cell proliferation in DG as measured by Ki67 + cell population, but CC3-positive cell numbers increased following EtOH or ACEA treatment suggesting an increase in cell death.
conclusionsTogether, these findings suggest that acute CB1R cannabinoid receptor activation and binge EtOH treatment reduce neurogenesis through mechanisms involving CB1R.
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