ArticleAlcoholism, clinical and experimental research2013
Cyclic adenosine monophosphate and brain-derived neurotrophic factor decreased oxidative stress and apoptosis in developing hypothalamic neuronal cells: role of microglia.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 71 citations in OpenAlex.
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- Preimplantational ethanol exposure causes disturbances in gene expression and abnormalities in cerebral cortex morphogenesis and behavior.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- GET73 modulates lipopolysaccharide- and ethanol-induced increase in cytokine/chemokine levels in primary cultures of microglia of rat cerebral cortex.Pharmacological reports : PR · 2024Article
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- Nicotinamide ameliorates mitochondria-related neuronal apoptosis and cognitive impairment via the NADSchizophrenia (Heidelberg, Germany) · 2023Article
- Nicotinamide reverses deficits in puberty-born neurons and cognitive function after maternal separation.Journal of neuroinflammation · 2022Article
- Alcohol-Induced Oxidative Stress and the Role of Antioxidants in Alcohol Use Disorder: A Systematic Review.Antioxidants (Basel, Switzerland) · 2022Review
- Exploring Hyperoxia Effects in Cancer-From Perioperative Clinical Data to Potential Molecular Mechanisms.Biomedicines · 2021Review
- Neuroinflammatory contribution of microglia and astrocytes in fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Review
- Involvement of Hepcidin in Cognitive Damage Induced by Chronic Intermittent Hypoxia in Mice.Oxidative medicine and cellular longevity · 2021Article
- Alcohol Increases Exosome Release from Microglia to Promote Complement C1q-Induced Cellular Death of Proopiomelanocortin Neurons in the Hypothalamus in a Rat Model of Fetal Alcohol Spectrum Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- dBcAMP Rescues the Neurons From Degeneration in Kainic Acid-Injured Hippocampus, Enhances Neurogenesis, Learning, and Memory.Frontiers in behavioral neuroscience · 2020Article
- A Physiologically Based Approach to Prescribing Exercise Following a Sport-Related Concussion.Sports medicine (Auckland, N.Z.) · 2019Review
- Chronic Binge Alcohol-Associated Differential Brain Region Modulation of Growth Factor Signaling Pathways and Neuroinflammation in Simian Immunodeficiency Virus-Infected Male Macaques.Alcohol and alcoholism (Oxford, Oxfordshire) · 2019Article
- Aging with alcohol-related brain damage: Critical brain circuits associated with cognitive dysfunction.International review of neurobiology · 2019Review
- Role of MCP-1 and CCR2 in alcohol neurotoxicity.Pharmacological research · 2019Review
- Role of MCP-1 and CCR2 in ethanol-induced neuroinflammation and neurodegeneration in the developing brain.Journal of neuroinflammation · 2018Article
- Impact of Alcohol on HIV Disease Pathogenesis, Comorbidities and Aging: Integrating Preclinical and Clinical Findings.Alcohol and alcoholism (Oxford, Oxfordshire) · 2018Review
- Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe have previously shown that ethanol (EtOH) increases cellular apoptosis to developing neurons via the effects on oxidative stress of neurons directly and via increasing production of microglia-derived factors. To study further the mechanism of EtOH action on neuronal apoptosis, we determined the effects of 2 well-known PKA activators, dibutyryl cAMP (dbcAMP) and brain-derived neurotrophic factor (BDNF), on EtOH-activated oxidative stress and apoptotic processes in the hypothalamic neurons in the presence and absence of microglial cells' influence.
methodsIn enriched neuronal cells from fetal rat hypothalami treated with EtOH or with conditioned medium from EtOH-treated microglia, we measured cellular apoptosis by the free nucleosome assay and the levels of cAMP, BDNF, O²⁻, reactive oxygen species (ROS), nitrite, glutathione (GSH), and catalase following treatment with EtOH or EtOH-treated microglial culture conditioned medium. Additionally, we tested the effectiveness of dbcAMP and BDNF in preventing EtOH or EtOH-treated microglial conditioned medium on cellular apoptosis and oxidative stress in enriched hypothalamic neuronal cell in primary cultures.
resultsNeuronal cell cultures following treatment with EtOH or EtOH-activated microglial conditioned medium showed decreased production levels of cAMP and BDNF. EtOH also increased apoptotic death as well as oxidative status, as demonstrated by higher cellular levels of oxidants but lower levels of antioxidants, in neuronal cells. These effects of EtOH on oxidative stress and cell death were enhanced by the presence of microglia. Treatment with BDNF or dbcAMP decreased EtOH or EtOH-activated microglial conditioned medium-induced changes in the levels of intracellular free radicals, ROS and O²⁻, nitrite, GSH, and catalase.
conclusionsThese data support the possibility that EtOH by acting directly and via increasing the production of microglial-derived factors reduces cellular levels of cAMP and BDNF to increase cellular oxidative status and apoptosis in hypothalamic neuronal cells in primary cultures.
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