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4. Pharmacological Depletion of Microglia Protects Against Alcohol-Induced Corticolimbic Neurodegeneration During Intoxication in Male Rats.

Author

Carlson, Erika R., Melbourne, Jennifer K., and Nixon, Kimberly

Abstract

Excessive alcohol use damages the brain, especially corticolimbic regions such as the hippocampus and rhinal cortices, leading to learning and memory problems. While neuroimmune reactivity is hypothesized to underly alcohol-induced damage, direct evidence of the causal role of microglia, brain-resident immune cells, in this process is lacking. Here, we depleted microglia using PLX5622 (PLX), a CSF1R inhibitor commonly used in mice, but rarely in rats, and assessed cell death following binge-like alcohol exposure in male rats. Eleven days of PLX treatment depleted microglia > 90%. Further, PLX treatment prevented alcohol-induced neuronal death in the hippocampus and rhinal cortices, as the number of FluoroJade-B-positive cells (dying neurons) was reduced to control diet levels. This study provides direct evidence that alcohol-induced microglial reactivity is neurotoxic in male rats. Improved understanding of alcohol-microglia interactions is essential for developing therapeutics that suppress pro-cytotoxic and/or amplify protective microglia activity to relieve alcohol-related damage. [ABSTRACT FROM AUTHOR]

Published
2025
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9. Chronic intermittent ethanol exposure during adolescence produces sex- and age-dependent changes in anxiety and cognition without changes in microglia reactivity late in life

Author

Matthews, Douglas B., primary, Scaletty, Samantha, additional, Trapp, Sarah, additional, Schreiber, Areonna, additional, Rossmann, Gillian, additional, Imhoff, Bailey, additional, Petersilka, Quinn, additional, Kastner, Abigail, additional, Pauly, Jim, additional, and Nixon, Kimberly, additional

Published
2023
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11. Neuroimmune Activation and Microglia Reactivity in Female Rats Following Alcohol Dependence.

Author

Melbourne, Jennifer K., Wooden, Jessica I., Carlson, Erika R., Anasooya Shaji, Chinchusha, and Nixon, Kimberly

Subjects
ALCOHOLISM, MICROGLIA, ETHANOL, RATS, BRAIN anatomy, FEMALES
Abstract

The rates of alcohol use disorder among women are growing, yet little is known about how the female brain is affected by alcohol. The neuroimmune system, and specifically microglia, have been implicated in mediating alcohol neurotoxicity, but most preclinical studies have focused on males. Further, few studies have considered changes to the microglial phenotype when examining the effects of ethanol on brain structure and function. Therefore, we quantified microglial reactivity in female rats using a binge model of alcohol dependence, assessed through morphological and phenotypic marker expression, coupled with regional cytokine levels. In a time- and region-dependent manner, alcohol altered the microglial number and morphology, including the soma and process area, and the overall complexity within the corticolimbic regions examined, but no significant increases in the proinflammatory markers MHCII or CD68 were observed. The majority of cytokine and growth factor levels examined were similarly unchanged. However, the expression of the proinflammatory cytokine TNFα was increased, and the anti-inflammatory IL-10, decreased. Thus, female rats showed subtle differences in neuroimmune reactivity compared to past work in males, consistent with reports of enhanced neuroimmune responses in females across the literature. These data suggest that specific neuroimmune reactions in females may impact their susceptibility to alcohol neurotoxicity and other neurodegenerative events with microglial contributions. [ABSTRACT FROM AUTHOR]

Published
2024
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49. ECTOPIC HIPPOCAMPAL NEUROGENESIS IN ADOLESCENT MALE RATS FOLLOWING ALCOHOL DEPENDENCE

Author

McClain, Justin A., Morris, Stephanie A., Marshall, S. Alexander, and Nixon, Kimberly

Subjects
Male, Doublecortin Protein, Ethanol, Neurogenesis, Central Nervous System Depressants, Enzyme-Linked Immunosorbent Assay, Hippocampus, Article, Rats, Substance Withdrawal Syndrome, Rats, Sprague-Dawley, Alcoholism, Disease Models, Animal, nervous system, Animals, Humans
Abstract

The adolescent hippocampus is highly vulnerable to alcohol-induced damage, which could contribute to their increased susceptibility to alcohol use disorders. Altered adult hippocampal neurogenesis represents one potential mechanism by which alcohol (ethanol) affects hippocampal function. Based on the vulnerability of the adolescent hippocampus to alcohol-induced damage, and prior reports of long-term alcohol-induced effects on adult neurogenesis, we predicted adverse effects on adult neurogenesis in the adolescent brain following abstinence from alcohol dependence. Thus, we examined neurogenesis in adolescent male rats during abstinence following a four-day binge model of alcohol dependence. Bromodeoxyuridine and Ki67 immunohistochemistry revealed a 2.2-fold increase in subgranular zone cell proliferation after 7 days of abstinence. Increased proliferation was followed by a 75% increase in doublecortin expression and a 56% increase in surviving bromodeoxyuridine-labeled cells 14 and 35 days post-ethanol exposure, respectively. The majority of newborn cells in ethanol and control groups co-localized with NeuN, indicating a neuronal phenotype and therefore a 1.6-fold increase in hippocampal neurogenesis during abstinence. Although these results mirror the magnitude of reactive neurogenesis described in adult rat studies, ectopic bromodeoxyuridine and doublecortin positive cells were detected in the molecular layer and hilus of adolescent rats displaying severe withdrawal symptoms, an effect that has not been described in adults. The presence of ectopic neuroblasts suggests that a potential defect exists in the functional incorporation of new neurons into the existing hippocampal circuitry for a subset of rats. Age-related differences in functional incorporation could contribute to the increased vulnerability of the adolescent hippocampus to ethanol.

Published
2013

50. Summary of the 2014 Alcohol and Immunology Research Interest Group (AIRIG) meeting

Author

Hammer, Adam M., primary, Morris, Niya L., additional, Cannon, Abigail R., additional, Shults, Jill A., additional, Curtis, Brenda, additional, Casey, Carol A., additional, Sueblinvong, Viranuj, additional, Persidsky, Yuri, additional, Nixon, Kimberly, additional, Brown, Lou Ann, additional, Waldschmidt, Thomas, additional, Mandrekar, Pranoti, additional, Kovacs, Elizabeth J., additional, and Choudhry, Mashkoor A., additional

Published
2015
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