A low chronic ethanol exposure induces morphological changes in the adolescent rat brain that are not fully recovered even after a long abstinence: An immunohistochemical study

Evrard, Sergio Gustavo; Vega, Maite Duhalde; Tagliaferro, Patricia; Mirochnic, Sebastián; Caltana, Laura; Brusco, Alicia

doi:10.1016/j.expneurol.2006.03.001

Cited by 68 publications

(69 citation statements)

References 91 publications

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“…This response is characterized by upregulation of the intermediate filament and astrocyte-specific marker, GFAP, as well as cellular hypertrophy and elongated processes. Astrocyte reactivity has been observed in multiple brain regions, including the frontal cortex, hippocampus and cerebellum of ethanol-exposed mice and rats [49,[83][84][85][86][87][88]. Differences in GFAP-positive astrocyte distributions in human brains have also been shown [89].…”

Section: Alcohol Induces Reactive Astrocytesmentioning

confidence: 99%

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

et al. 2016

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Transcriptome profiling enables discovery of gene networks that are altered in alcoholic brains. This technique has revealed involvement of the brain's neuroimmune system in regulating alcohol abuse and dependence, and has provided potential therapeutic targets. In this review, we discuss Toll-like-receptor pathways, hypothesized to be key players in many stages of the alcohol addiction cycle. The growing appreciation of the neuroimmune system's involvement in alcoholism has also led to consideration of crucial roles for glial cells, including astrocytes and microglia, in the brain's response to alcohol abuse. We discuss current knowledge and hypotheses on the roles that specific neuroimmune cell types may play in addiction. Current strategies for repurposing US FDA-approved drugs for the treatment of alcohol use disorders are also discussed.

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Section: Alcohol Induces Reactive Astrocytesmentioning

confidence: 99%

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

et al. 2016

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“…Fetal alcohol exposure clearly contributes to physical anomalies in humans 14 and animals. 17 Animal research has shown that repeated alcohol exposure during adolescence induces inflammatory cell death, 26 as well as morphologic and neurochemical changes in the brain that may persist into adulthood, 27,28 although studies have yet to explore whether adults would be less vulnerable to these effects than adolescents. Research with human adolescents indicates that severe AUD is associated with reduced hippocampal volume, 29,30 although these results should not be interpreted as necessarily being causal.…”

Section: Development Itself May Be Altered By Alcohol Exposurementioning

confidence: 99%

Underage Drinking: A Developmental Framework

et al. 2008

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A developmental framework for understanding and addressing the problem of underage alcohol consumption is presented. The first section presents the rationale for a developmental approach, including striking age-related data on patterns of onset, prevalence, and course of alcohol use and disorders in young people. The second section examines the fundamental meaning of a developmental approach to conceptualizing underage drinking. The third section delineates contemporary principles of developmental psychopathology as a guide to future research and intervention efforts. Strategic, sensitive, and effective efforts to address the problem of underage drinking will require a developmentally informed approach to research, prevention, and treatment. D EVELOPMENTAL APPROACHES TO understanding and addressing the problem of underage drinking are essential, not only because this problem occurs in a developing organism but also because accumulating evidence strongly implicates the role of development in promising theories and interventions concerning this problem. It is increasingly clear that the emergence and progression of drinking behavior are influenced by development, that underage drinking has developmental consequences, that alcohol use disorders (AUDs) are developmental in nature, and that efforts to prevent or to reduce underage drinking behavior must be developmentally informed to be strategic, sensitive, and effective. Our goals in this article are to summarize the case for a developmental perspective on underage drinking and to outline a developmental framework for underage drinking, to guide future theory, research, and practice. This framework emerged from the collaborative work of an advisory group assembled by the National Institute on Alcohol Abuse and Alcoholism in 2004 as part of the Underage Drinking Research Initiative.The framework is presented in 3 sections. In the first section, we highlight the rationale for a developmental approach, including examples of data that the advisory group members found compelling as a rationale for developmental perspectives. In the second section, we discuss general developmental principles that guided our thinking, with examples of their application to drinking behavior. In the third section, we articulate principles of contemporary developmental psychopathology as applied to the problem of underage drinking. RATIONALE FOR A DEVELOPMENTAL APPROACH TO UNDERAGE DRINKING FocusWhen the evidence on drinking behavior is examined through a developmental lens, the rationale for a developmental approach to understanding and preventing this problem comes into focus. In this section, we highlight conclusions based on the most salient data supporting a developmental approach.There Are Striking Age-Related Patterns of Alcohol Use, Problems, Abuse, and Dependence Alcohol use typically begins in the second decade of life, often in early adolescence. Although some young people begin drinking in elementary school, the first use of alcohol (defined as drinking a whole drink) typ...

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“…Earlier, correlations between a considerable drop in the content of the IF protein, destruction of the cytoskeletal network in neurons, and arrival of axons and dendrites with aberrant morphology under conditions of long-lasting action of ethanol were demonstrated [31]. Chronic consumption of ethanol is also accompanied by degradation of IFs (structures that are rather stable constructions in the norm) and crucial changes in morphology of glial cells, which do not recover even after a long rehabilitation period [11]. These changes in the cytoskeleton of different cells of the nerve tissue can be determined by a few reasons.…”

Section: Discussionmentioning

confidence: 96%

“…Loss of the IF proteins is accompanied by the arrival of aberrant axons and dendrites in brain tissues of alcoholized animals, and also by destructive changes in the morphology of glial cells. In the latter cells, such changes are not fully recovered even after a long abstinence period [11]. Disturbances in the metabolism of IF proteins and in the dynamic equilibrium of the intracellular filamental system, cytoarchitectonics, and cell morphology of neurons and glia in mammals correlate with disorders in the behavioral, emotional, and cognitive activity [12].…”

Section: Introductionmentioning

confidence: 99%

Disorders in the Cytoskeleton of Astroglia and Neurons in the Rat Brain Induced by Long-Lasting Exposure to Ethanol and Correction of These Shifts by Hydrated Fullerene С60

2008

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Using an immunoblotting technique, we examined the content of proteins of intermediate filaments of the cytoskeleton of neurons and astroglial cells and also changes in the polypeptide composition of these proteins in different brain regions of rats subjected to long-term (12 weeks) alcoholization. The sensitivity of these indices to the effect of ethanol in different cerebral structures was in the following sequence: hippocampus > cerebral cortex > cerebellum. The greatest changes in a marker of the astrocyte cytoskeleton (glial fibrillary acidic protein, GFAP) were observed in the hippocampus of alcoholized animals, where the GFAP level was by 72% lower with respect to the control values. In this cerebral region, the content of the neurofilament 210-kdalton subunit also sharply dropped (by 76% with respect to the control). A positive correlation between a decrease in the GFAP content and loss of the neurofilament 210-kdalton subunit was demonstrated. These data show that the organization of the intracellular filamentary system of neurons and gliocytes is disturbed under experimental conditions, and this is one of the probable reasons for cell death in the nerve tissue induced by chronic consumption of ethanol. The use of a hydrated form of fullerene С 60 (its molecular/colloid solution) for antioxidant correction of the pathological state of the CNS induced by the above-mentioned toxicant removed, to a considerable extent, negative modifications of cytoskeletal structures and protected astroglial and nerve cells from degeneration.

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A low chronic ethanol exposure induces morphological changes in the adolescent rat brain that are not fully recovered even after a long abstinence: An immunohistochemical study

Cited by 68 publications

References 91 publications

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

Underage Drinking: A Developmental Framework

Disorders in the Cytoskeleton of Astroglia and Neurons in the Rat Brain Induced by Long-Lasting Exposure to Ethanol and Correction of These Shifts by Hydrated Fullerene С60

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