scholarly journals Aberrations in Incentive Learning and Responding to Heroin in Male Rats After Adolescent or Adult Chronic Binge‐Like Alcohol Exposure

2020 ◽  
Vol 44 (6) ◽  
pp. 1214-1223 ◽  
Author(s):  
Ewa Galaj ◽  
Eddy Barrera ◽  
Debra Morris ◽  
Yao‐Ying Ma ◽  
Robert Ranaldi
Keyword(s):  
Alcohol Exposure ◽  
Male Rats ◽  
Incentive Learning

scholarly journals Moderate prenatal alcohol exposure impairs performance by adult male rats in an object-place paired-associate task

2019 ◽  
Vol 360 ◽  
pp. 228-234 ◽  
Author(s):  
Lilliana M. Sanchez ◽  
Jonathan Goss ◽  
Jennifer Wagner ◽  
Suzy Davies ◽  
Daniel D. Savage ◽  
...  
Keyword(s):  
Adult Male ◽  
Paired Associate ◽  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Male Rats ◽  
Prenatal Alcohol

Effect of prenatal stress on alcohol preference and sensitivity to chronic alcohol exposure in male rats

2010 ◽  
Vol 214 (1) ◽  
pp. 197-208 ◽  
Author(s):  
Vincent Van Waes ◽  
Mihaela Enache ◽  
Olivier Berton ◽  
Elisabeth Vinner ◽  
Michel Lhermitte ◽  
...  
Keyword(s):  
Prenatal Stress ◽  
Alcohol Exposure ◽  
Alcohol Preference ◽  
Male Rats ◽  
Chronic Alcohol ◽  
Chronic Alcohol Exposure

Acute and chronic effects of alcohol exposure on skeletal muscle c-myc, p53, and Bcl-2 mRNA expression

2003 ◽  
Vol 285 (6) ◽  
pp. E1273-E1281 ◽  
Author(s):  
Tatsuo Nakahara ◽  
Kijiro Hashimoto ◽  
Makoto Hirano ◽  
Michael Koll ◽  
Colin R. Martin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Internal Standard ◽  
Alcohol Exposure ◽  
Female Rats ◽  
Male Rats ◽  
Skeletal Muscle Atrophy ◽  
Muscle Pathology ◽  
Mrna Levels ◽  
Male And Female Rats

Skeletal muscle atrophy is a common feature in alcoholism that affects up to two-thirds of alcohol misusers, and women appear to be particularly susceptible. There is also some evidence to suggest that malnutrition exacerbates the effects of alcohol on muscle. However, the mechanisms responsible for the myopathy remain elusive, and some studies suggest that acetaldehyde, rather than alcohol, is the principal pathogenic perturbant. Previous reports on rats dosed acutely with ethanol (<24 h) have suggested that increased proto-oncogene expression (i.e., c-myc) may be a causative process, possibly via activating preapoptotic or transcriptional pathways. We hypothesized that 1) increases in c-myc mRNA levels also occur in muscle exposed chronically to alcohol, 2) muscle of female rats is more sensitive than that from male rats, 3) raising acetaldehyde will also increase c-myc, 4) prior starvation will cause further increases in c-myc mRNA expression in response to ethanol, and 5) other genes involved in apoptosis (i.e., p53 and Bcl-2) would also be affected by alcohol. To test this, we measured c-myc mRNA levels in skeletal muscle of rats dosed either chronically (6–7 wk; ethanol as 35% of total dietary energy) or acutely (2.5 h; ethanol as 75 mmol/kg body wt ip) with ethanol. All experiments were carried out in male Wistar rats (∼0.1–0.15 kg body wt) except the study that examined gender susceptibility in male and female rats. At the end of the studies, rats were killed, and c-myc, p53, and Bcl-2 mRNA was analyzed in skeletal muscle by RT-PCR with an endogenous internal standard, GAPDH. The results showed that 1) in male rats fed ethanol chronically, there were no increases in c-myc mRNA; 2) increases, however, occurred in c-myc mRNA in muscle from female rats fed ethanol chronically; 3) raising endogenous acetaldehyde with cyanamide increased c-myc mRNA in acute studies; 4) starvation per se increased c-myc mRNA levels and at 1 day potentiated the acute effects of ethanol, indicative of a sensitization response; 5) the only effect seen with p53 mRNA levels was a decrease in muscle of rats starved for 1 day compared with fed rats, and there was no statistically significant effect on Bcl-2 mRNA in any of the experimental conditions. The increases in c-myc may well represent a preapoptotic effect, or even a nonspecific cellular stress response to alcohol and/or acetaldehyde. These data are important in our understanding of a common muscle pathology induced by alcohol.

Abstract 123: Increased Susceptibility of Mitochondria to Permeability Transition Pore Opening in Alcoholic Cardiomyopathy

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Larisa Emelyanova ◽  
Ekhson Holmuhamedov ◽  
Sean Ryan ◽  
Kelsey Kraft ◽  
Stacie Edwards ◽  
...  
Keyword(s):  
Adenine Nucleotide ◽  
Myocardial Dysfunction ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Alcohol Exposure ◽  
Male Rats ◽  
Voltage Dependent Anion Channel ◽  
Alcoholic Cardiomyopathy ◽  
Mptp Opening ◽  
The Impact

Introduction: Although generations of reactive oxygen species and mitochondrial dysfunction have been implicated in pathogenesis of alcoholic cardiomyopathy (ACM), molecular target(s) responsible for myocardial dysfunction in ACM are not well known. Objective: To determine the impact of chronic alcohol exposure on mitochondrial oxidative phosphorylation system (OXPHOS), permeability transition pore (mPTP) opening, and oxidative stress using a rat model of ACM. Methods: Sprague Dawley male rats (1 mo old) were exposed to alcohol (7.5% ethanol) for 3 months to develop ACM. Activity of OXPHOS was assessed enzymatically and by measuring mitochondrial oxygen consumption rate (OCR). The mPTP opening was determined by monitoring abrupt release of Ca 2+ after exposure of mitochondria to Ca 2+ . Western blot and RT-PCR were used to assess the expression of OXPHOS and mPTP protein components and corresponding genes. Malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were determined in heart tissue homogenates. Results: There was no significant change in OCR or activity of OXPHOS complexes I-V, despite a decrease in complex V protein and Atp6v1e2 gene expression (-1.7-fold, p<0.01) in Alc rats. Mitochondria from Alc rats were more sensitive to Ca 2+ -induced mPTP opening. This was associated with increase in protein expression level of adenine nucleotide translocase 1/2 and voltage dependent anion channel 1. There was no difference in MDA or 4-HNE levels. Conclusion: Increased sensitivity of mitochondria to mPTP opening during long-term alcohol consumption may compromise cardiac energetic reserves and contractility, leading to ACM development and progression.

Selective and Enduring Deficits in Spatial Learning After Limited Neonatal Binge Alcohol Exposure in Male Rats

2002 ◽  
Vol 26 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Timothy B. Johnson ◽  
Charles R. Goodlett
Keyword(s):  
Spatial Learning ◽  
Alcohol Exposure ◽  
Male Rats

scholarly journals Type 2 Neural Progenitor Cell Activation Drives Reactive Neurogenesis after Binge-Like Alcohol Exposure in Adolescent Male Rats

2017 ◽  
Vol 8 ◽  
Author(s):  
Chelsea R. Geil Nickell ◽  
Hui Peng ◽  
Dayna M. Hayes ◽  
Kevin Y. Chen ◽  
Justin A. McClain ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Cell Activation ◽  
Alcohol Exposure ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Male Rats ◽  
Adolescent Male

Prenatal Alcohol Exposure Causes Attention Deficits in Male Rats.

2005 ◽  
Vol 119 (1) ◽  
pp. 302-310 ◽  
Author(s):  
Kathryn A. Hausknecht ◽  
Ashley Acheson ◽  
Andrew M. Farrar ◽  
Artur K. Kieres ◽  
Roh-Yu Shen ◽  
...  
Keyword(s):  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Attention Deficits ◽  
Male Rats ◽  
Prenatal Alcohol

scholarly journals Recovery of Hippocampal-Dependent Learning Despite Blunting Reactive Adult Neurogenesis After Alcohol Dependence

2020 ◽  
Vol 6 (1) ◽  
pp. 83-101 ◽  
Author(s):  
Chelsea G. Nickell ◽  
K. Ryan Thompson ◽  
James R. Pauly ◽  
Kimberly Nixon
Keyword(s):  
Alcohol Dependence ◽  
Adult Neurogenesis ◽  
Alcohol Exposure ◽  
Cell Number ◽  
Male Rats ◽  
Proliferating Cells ◽  
Excessive Alcohol ◽  
Reactive Proliferation ◽  
Dependent Learning

Background: The excessive alcohol drinking that occurs in alcohol use disorder (AUD) causes neurodegeneration in regions such as the hippocampus, though recovery may occur after a period of abstinence. Mechanisms of recovery are not clear, though reactive neurogenesis has been observed in the hippocampal dentate gyrus following alcohol dependence and correlates to recovery of granule cell number. Objective: We investigated the role of neurons born during reactive neurogenesis in the recovery of hippocampal learning behavior after 4-day binge alcohol exposure, a model of an AUD. We hypothesized that reducing reactive neurogenesis would impair functional recovery. Methods: Adult male rats were subjected to 4-day binge alcohol exposure and two approaches were tested to blunt reactive adult neurogenesis, acute doses of alcohol or the chemotherapy drug, temozolomide (TMZ). Results: Acute 5 g/kg doses of EtOH gavaged T6 and T7 days post binge did not inhibit significantly the number of Bromodeoxyuridine-positive (BrdU+) proliferating cells in EtOH animals receiving 5 g/kg EtOH versus controls. A single cycle of TMZ inhibited reactive proliferation (BrdU+ cells) and neurogenesis (NeuroD+ cells) to that of controls. However, despite this blunting of reactive neurogenesis to basal levels, EtOH-TMZ rats were not impaired in their recovery of acquisition of the Morris water maze (MWM), learning similarly to all other groups 35 days after 4-day binge exposure. Conclusions: These studies show that TMZ is effective in decreasing reactive proliferation/neurogenesis following 4-day binge EtOH exposure, and baseline levels of adult neurogenesis are sufficient to allow recovery of hippocampal function.

scholarly journals Microglia Dystrophy Following Binge-Like Alcohol Exposure in Adolescent and Adult Male Rats

2020 ◽  
Vol 14 ◽  
Author(s):  
S. Alex Marshall ◽  
Justin A. McClain ◽  
Jessica I. Wooden ◽  
Kimberly Nixon
Keyword(s):  
Adult Male ◽  
Alcohol Exposure ◽  
Male Rats

scholarly journals Impact of adolescent intermittent ethanol exposure on interneurons and their surrounding perineuronal nets in adulthood.

2022 ◽  
Author(s):  
Carol A. Dannenhoffer ◽  
Alex Gómez-A ◽  
Victoria Macht ◽  
Rayyanoor Jawad ◽  
E. Blake Sutherland ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Behavioral Flexibility ◽  
Alcohol Exposure ◽  
Ethanol Exposure ◽  
Male Rats ◽  
Perineuronal Nets ◽  
Cholinergic Interneurons ◽  
Medial Pfc ◽  
Behavioral Impairments ◽  
Brain And Behavior

Background: Binge alcohol exposure during adolescence results in long-lasting alterations in brain and behavior. For example, adolescent intermittent ethanol (AIE) exposure in rodents results in long-term loss of functional connectivity among prefrontal cortex (PFC) and striatal regions as well as a variety of neurochemical, molecular, and epigenetic alterations. Interneurons in the PFC and striatum play critical roles in behavioral flexibility and functional connectivity. For example, parvalbumin (PV) interneurons are known to contribute to neural synchrony, and cholinergic interneurons contribute to strategy selection. Furthermore, extracellular perineuronal nets (PNNs) surround some interneurons, particularly PV+ interneurons, to further regulate cellular plasticity. The effect of AIE exposure on expression of these markers within the PFC is not well understood. Methods: The present study tested the hypothesis that AIE exposure reduces expression of PV+ and ChAT+ interneurons in the adult PFC and striatum and increases related expression of PNNs (marked by binding of Wisteria Floribunda agglutinin lectin; WFA) in adulthood. Male rats were exposed to AIE (5 g/kg/day, 2-days-on/2-days-off, i.g., P25-P54) or water (CON), and brain tissue was harvested in adulthood (> P80). Immunohistochemistry and co-immunofluorescence were used to assess expression of ChAT, PV, and WFA labeling within the adult PFC and striatum following AIE exposure. Results: ChAT and PV interneuron numbers in the striatum and PFC were unchanged after AIE exposure. However, WFA labeling in the PFC of AIE-exposed rats was increased compared to CON rats. Moreover, significantly more PV neurons were surrounded by WFA labeling in AIE-exposed subjects relative to controls in both PFC subregions assessed: the orbitofrontal cortex (CON = 34%; AIE = 40%) and the medial PFC (CON = 10%; AIE = 14%). Conclusions: These findings indicate that while PV interneuron expression in the adult PFC and striatum is unaltered following AIE exposure, PNNs surrounding these neurons (indicated by extracellular WFA binding) are increased. This increase in PNNs may restrict plasticity of the ensheathed neurons, thus contributing to impaired microcircuitry in frontostriatal connectivity and related behavioral impairments.

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