Repeated cycles of binge-like ethanol exposure induce immediate and delayed neurobehavioral changes and hippocampal dysfunction in adolescent female rats

Fernandes, Luanna Melo Pereira; Cartágenes, Sabrina C.; Barros, Mayara A.; Carvalheiro, T.C. Vilhena; Castro, Nair C.F.; Schamne, Marissa Giovanna; Lima, Rafael Rodrigues; Prediger, Rui Daniel; Monteiro, Marta Chagas; Fontes-Júnior, Enéas Andrade; Cunha, Rodrigo A.; Maia, Cristiane do Socorro Ferraz

doi:10.1016/j.bbr.2018.05.007

Cited by 33 publications

(49 citation statements)

References 68 publications

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“…These results contrasted with those about binge‐like ethanol exposure in adolescent female rats (Fernandes et al . ) and those about short (15 days) ethanol exposure and 3–11 days of withdrawal in the hippocampus of adult rats (Alele and Devaud ; Schunck et al . ).…”

Section: Discussionmentioning

confidence: 99%

Alcohol‐induced cognitive deficits are associated with decreased circulating levels of the neurotrophin BDNF in humans and rats

et al. 2018

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Chronic alcohol consumption is associated with neurocognitive and memory deficits, dramatically affecting plasticity and connectivity, with maximal expression as dementia. Neurotrophic factors may contribute to alcohol-related cognitive decline. For further investigation, a cross-sectional study was performed to evaluate the association of cognitive impairment, by using frontal assessment battery, and memory loss, using memory failures everyday, with the circulating levels of the neurotrophin brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) in abstinent subjects with alcohol use disorders (AUDs, N = 58, average of 17.9 years of problematic use and 4.3 months of abstinence) compared with healthy control subjects (N = 22). This association was also explored in a pre-clinical model of adolescent rats chronically exposed to alcohol up to adulthood (~77 days old) in a three-bottle free-choice (5-10-20 percent), repeated abstinence and relapse paradigm. AUD subjects had low educational level and cognitive impairment associated with teenage consumption and lower circulating levels of BDNF and NT-3. Only BDNF concentration showed a positive correlation with frontal assessment battery in AUD patients. In the ethanol-exposed rats, the plasma levels of BDNF and NT-3 were also decreased, and a negative correlation between hippocampal Bdnf mRNA levels and recognition memory was found. The ethanol-exposed rat hippocampus showed a decrease in the mRNA levels of neurotrophic (Bdnf and Ntf-3) and neurogenic (Mki67, Sox2, Dcx, Ncam1 and Calb1) factors, associated to a deactivation of the neurogenic regulator mitogen-activated protein kinase extracellular signal-regulated kinase. Results suggest a relevant role of BDNF/extracellular signal-regulated kinase 2 signaling in alcohol-induced cognitive impairment and suggest that early alcohol exposure-derived effects on cognition are associated with neurotrophin signaling deficits.

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Section: Discussionmentioning

confidence: 99%

Alcohol‐induced cognitive deficits are associated with decreased circulating levels of the neurotrophin BDNF in humans and rats

et al. 2018

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“…Three groups were used: control, untreated, and treated individuals. The treated and untreated groups were exposed to 5 binges (beginning at 35 days old) of ethanol (3 g/kg/day; 20% w / v ), which consists the middle adolescence until the adult phase [ 10 ]. This binge-drinking paradigm reaches a BAC of approximately 250 mg/dL [ 10 ], which reflects the binge-drinking pattern (over 80 mg/dL; [ 8 ]).…”

Section: Methodsmentioning

confidence: 99%

“…The treated and untreated groups were exposed to 5 binges (beginning at 35 days old) of ethanol (3 g/kg/day; 20% w / v ), which consists the middle adolescence until the adult phase [ 10 ]. This binge-drinking paradigm reaches a BAC of approximately 250 mg/dL [ 10 ], which reflects the binge-drinking pattern (over 80 mg/dL; [ 8 ]). Twenty-four hours after the last binge administration, animals received AEGl (treated) or distilled water (untreated) for three consecutive days ( Figure 1 ).…”

Section: Methodsmentioning

confidence: 99%

“…Binge drinking is a pattern that consists of acute intoxication, i.e., 5 or more doses for men and 4 or more doses for women, during a short period of 2 hours, approximately, reaching a minimum blood alcohol concentration (BAC) of 80 mg/dL [ 6 – 8 ]. Previous researches carried out by our group have demonstrated that binge drinking pattern during adolescence modifies behavioral profiles, as spontaneous locomotion and motor coordination, as well as displays psychiatry-like and cognitive disorders, as anxiogenic and depressive phenotype, and memory impairment, associated to reduction-oxidation reactions (REDOX) imbalance in rodents [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Ganoderma lucidumAmeliorates Neurobehavioral Changes and Oxidative Stress Induced by Ethanol Binge Drinking

Nascimento

Luz

Silva

et al. 2020

Oxidative Medicine and Cellular Longevity

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Ganoderma lucidum, mushroom used for centuries by Asian peoples as food supplement, has been shown interesting biological activities, including over the Central Nervous System. Besides, these mushroom bioactive compounds present antioxidant and anti-inflammatory activities. On the side, binge drinking paradigm consists of ethanol exposure that reflects the usual consumption of adolescents, which elicits deleterious effects, determined by high ethanol consumption, in a short period. In this study, we investigated whether the Aqueous Extract of G. lucidum (AEGl) reduces the behavioral disorders induced by alcohol. Male (n=30) and female Wistar rats (n=40), seventy-two days old, were used for behavioral/biochemical and oral toxicity test, respectively. Animals were exposed to 5 binges (beginning at 35 days old) of ethanol (3 g/kg/day) or distilled water. Twenty-four hours after the last binge administration, animals received AEGl (100 mg/kg/day) or distilled water for three consecutive days. After treatment protocol, open field, elevated plus maze, forced swim, and step-down inhibitory avoidance tests were performed. Oxidative stress parameters were measured to evaluate the REDOX balance. Our results demonstrated that AEGl elicited the recovery of spontaneous horizontal exploration capacity, anxiogenic- and depressive-profile, as well as short-term memory damage induced by binge-ethanol exposure. The behavioral effects of the extract were associated to the reequilibrium of the animals’ REDOX balance. Thus, AEGl, a medicinal mushroom, ameliorates behavioral alteration on a model of motor, cognitive and psychiatric-like disorders induced by binge drinking paradigm and emerges as a useful tool as a food supplement in the management of disorders of alcoholic origin.

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“…The binge-like protocols trigger adverse effects on the central nervous system function and can produce significant consequences over time (Merrill and Carey, 2016;Tapia-Rojas et al, 2017). The binge-like alcohol treatment induced an impairment of spatial processing and recognition memory even at 1 week later from the binge episode, while cognitive performance is re-established at 10 weeks later from the binge episode (Silvestre de Ferron et al, 2016;Tapia-Rojas et al, 2018) or as soon as 14 days from ethanol withdrawal in a binge drinking model in female rats (Fernandes et al, 2018). The re-establishment of recognition memory performance has been recorded as soon as 3 weeks after the last alcohol exposure in a binge-like paradigm (Tapia-Rojas et al, 2018).…”

Section: Alcohol Consumption In Young Rodentsmentioning

confidence: 99%

Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission

Mira

Lira

Tapia-Rojas

et al. 2020

Front. Behav. Neurosci.

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Problematic alcohol drinking and alcohol dependence are an increasing health problem worldwide. Alcohol abuse is responsible for approximately 5% of the total deaths in the world, but addictive consumption of it has a substantial impact on neurological and memory disabilities throughout the population. One of the better-studied brain areas involved in cognitive functions is the hippocampus, which is also an essential brain region targeted by ethanol. Accumulated evidence in several rodent models has shown that ethanol treatment produces cognitive impairment in hippocampal-dependent tasks. These adverse effects may be related to the fact that ethanol impairs the cellular and synaptic plasticity mechanisms, including adverse changes in neuronal morphology, spine architecture, neuronal communication, and finally an increase in neuronal death. There is evidence that the damage that occurs in the different brain structures is varied according to the stage of development during which the subjects are exposed to ethanol, and even much earlier exposure to it would cause damage in the adult stage. Studies on the cellular and cognitive deficiencies produced by alcohol in the brain are needed in order to search for new strategies to reduce alcohol neuronal toxicity and to understand its consequences on memory and cognitive performance with emphasis on the crucial stages of development, including prenatal events to adulthood.

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Repeated cycles of binge-like ethanol exposure induce immediate and delayed neurobehavioral changes and hippocampal dysfunction in adolescent female rats

Cited by 33 publications

References 68 publications

Alcohol‐induced cognitive deficits are associated with decreased circulating levels of the neurotrophin BDNF in humans and rats

Alcohol‐induced cognitive deficits are associated with decreased circulating levels of the neurotrophin BDNF in humans and rats

Ganoderma lucidumAmeliorates Neurobehavioral Changes and Oxidative Stress Induced by Ethanol Binge Drinking

Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission

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