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Although most cognitive impairments induced by prolonged alcohol consumption tend to improve within the initial months of abstinence, there is evidence suggesting certain cognitive deficits may persist. This study aimed to investigate the impact of aerobic exercise on learning and memory in alcohol use disorder (AUD) mice following a period of abstinence from alcohol. We also sought to assess the levels of monoamine neurotransmitters in the hippocampus. To this end, we established an AUD mouse model through a two-bottle choice (sucrose fading mode and normal mode) and chronic intermittent alcohol vapor (combined with intraperitoneal injection) and randomly allocated mice into exercise groups to undergo treadmill training. Learning and memory abilities were assessed through the Morris water maze test and spontaneous activity was evaluated using the open field test. The levels of dopamine, norepinephrine, serotonin, and brain-derived neurotrophic factor in the hippocampus were quantified using enzyme-linked immunoassay (ELISA) kits. The findings reveal that after cessation of alcohol consumption, learning and memory abilities in AUD mice did not completely return to normal levels. The observed enhancement of cognitive functions in AUD mice through aerobic exercise may be attributed to restoring levels of monoamine neurotransmitters in the hippocampus, boosting brain-derived neurotrophic factor (BDNF) concentrations, and facilitating an increase in hippocampal mass. These results offer empirical evidence to support aerobic exercise as a viable therapeutic strategy to alleviate cognitive deficits associated with AUD.
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With the increases in work environment regulations restricting alcohol to 1000 ppm, and in drink-driving laws, testing for alcohol with a simple method is a crucial issue. Conventional alcohol sensors based on sulfide, metal oxide, boron nitride or graphene oxide have a detection limit in the range of 50-1000 ppm but have disadvantages of complicated manufacture and longer processing times. A recent portable alcohol meter based on semiconductor material using conductivity or chemistry measurements still has the problem of a complex and lengthy manufacturing process. In this paper, a simple and effective resistive-type alcohol vapor sensor using one-step anodic aluminum oxide (AAO) is proposed. The nanoporous AAO was produced in one-step by anodizing low-purity AA1050 at room temperature of 25 °C, which overcame the traditional high-cost and lengthy process at low temperature of anodization and etching from high-purity aluminum. The highly specific surface area of AAO has benefits for good sensing performance, especially as a humidity or alcohol vapor sensor. With the resistance measurement method, alcohol vapor concentration of 0, 100, 300, 500, 700 and 1000 ppm correspond to mean resistances of 8524 Ω, 8672 Ω, 9121 Ω, 9568 Ω, 10,243 Ω, and 11,045 Ω, respectively, in a linear relationship. Compared with other materials for detecting alcohol vapor, the AAO resistive sensor has advantages of fast and simple manufacturing with good detection limits for practical applications. The resistive-type alcohol vapor-sensing mechanism is described with respect to the resistivity of the test substance and the pore morphology of AAO. In a human breath test, the AAO sensor can quickly distinguish whether the subject is drinking, with normal breath response of -30% to -40% and -20% to -30% response after drinking 50 mL of wine of 25% alcohol.
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Alcohol use disorder (AUD) is a complex disorder characterized by compulsive alcohol use and a lack of control over alcohol intake. Several experimental methods using mouse models have been developed to improve research regarding this disorder. Mouse behavioral paradigms are advantageous in inducing alcohol dependence and evaluating alcohol intake, circumventing ethical issues, and increasing experimental control over human-based experiments. These behavioral methods typically fall under one of two categories: forced exposure and voluntary consumption. This paper highlights two common paradigms used to study AUD in rodent models: one forced exposure method (use of a vapor inhalation system for alcohol exposure) and one voluntary consumption method (the two-bottle choice procedure). The effectiveness and experimental validity of these behavioral paradigms for pathophysiological investigations of AUD and how they can be combined are also discussed, along with their individual strengths and weaknesses. © 2023 The Authors. Current Protocols published by Wiley Periodicals LLC. Basic Protocol 1: Vapor inhalation for exposure to alcohol Basic Protocol 2: Intermittent access two-bottle choice procedure (acquisition) Basic Protocol 3: Intermittent access two-bottle choice procedure (measurement) Alternate Protocol: Sucrose fading to encourage voluntary alcohol consumption.
Asunto(s)
Alcoholismo , Humanos , Ratones , Animales , Consumo de Bebidas Alcohólicas , Etanol/farmacología , Administración por Inhalación , Modelos TeóricosRESUMEN
An increasing number of studies demonstrated that alcohol vapor chamber is an effective way to model physical signs of alcohol use disorders. Although researchers are developing different vapor chambers to study chronic alcohol exposure model worldwide, few studies build and modify their own vapor chambers in China. Here, we designed and established an alcohol vapor chamber system for small animals. We described a paradigm showing how to control and monitor alcohol concentration in whole system. The vapor chamber system with several advantages including accommodating up to ten standard mouse cages. Furthermore, the system was tested by evaluating the blood alcohol concentration and neuron injury in mice. Importantly, the alcohol withdrawal after vapor exposure caused motor coordination impairment, anxiolytic- and depression-like behavior. Finally, the N-methyl-D-aspartate receptor (NMDAR)-mediated glutamatergic transmissions in the medial prefrontal cortex was changed after alcohol vapor exposure-induced behaviors. The frequency and amplitude of spontaneous excitatory postsynaptic currents between control and alcohol groups were not different, suggesting that alcohol exposure-induced behaviors are associated with the change in NMDAR response. Taken together, the new alcohol vapor chamber system was constructed, which would help to research the relationship between the stable alcohol exposure and withdrawal behaviors and to study chronic alcohol exposure-induced disorders in China.
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Alcohol dependence is associated with adverse consequences of alcohol (ethanol) use and is evident in most severe cases of alcohol use disorder (AUD). The central nucleus of the amygdala (CeA) plays a critical role in the development of alcohol dependence and escalation of alcohol consumption in dependent subjects. Molecular mechanisms underlying the CeA-driven behavioral changes are not well understood. Here, we examined the effects of alcohol on global gene expression in the CeA using a chronic intermittent ethanol (CIE) vapor model in rats and RNA sequencing (RNA-Seq). The CIE procedure resulted in robust changes in CeA gene expression during intoxication, as the number of differentially expressed genes (DEGs) was significantly greater than those expected by chance. Over-representation analysis of cell types, functional groups and molecular pathways revealed biological categories potentially important for the development of alcohol dependence in our model. Genes specific for astrocytes, myelinating oligodendrocytes, and endothelial cells were over-represented in the DEG category, suggesting that these cell types were particularly affected by the CIE procedure. The majority of the over-represented functional groups and molecular pathways were directly related to the functions of glial and endothelial cells, including extracellular matrix (ECM) organization, myelination, and the regulation of innate immune response. A coordinated regulation of several ECM metalloproteinases (e.g., Mmp2; Mmp14), their substrates (e.g., multiple collagen genes and myelin basic protein; Mbp), and a metalloproteinase inhibitor, Reck, suggests a specific mechanism for ECM re-organization in response to chronic alcohol, which may modulate neuronal activity and result in behavioral changes, such as an escalation of alcohol drinking. Our results highlight the importance of glial and endothelial cells in the effects of chronic alcohol exposure on the CeA, and demonstrate further insight into the molecular mechanisms of alcohol dependence in rats. These molecular targets may be used in future studies to develop therapeutics to treat AUD.
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Solvothermal reaction of zinc meso-tetra(4-carboxyphenyl)porphyrin and 2,6-diaminopurine with zinc salt in DMF affords a three-dimensional bioMOF (1-α). Its infinite rod-shaped building block features an alternation of octahedral Zn4O and paddle-wheel Zn2 clusters bridged by 2,6-diaminopurines. The paddle-wheel Zn2 cluster undergoes reversible transformation with half into quasi-paddle-wheel Zn2 cluster and the other half into two tetrahedral mononuclear clusters upon release/uptake of guest molecules, resulting in a new phase 1-ß. This single-crystal to single-crystal transformation is accompanied by luminescence on/off switching, possibly associated with the structural conversion between the porphyrin-ligand-based photoactive 1-α and the porphyrin-stacking-caused non-photoactive 1-ß. Interestingly, 1-ß exhibits quick luminescence turn-on in alcohol vapor instead of other volatile organic solvents by transforming into an intermediate phase 1-γ, which shows a partial luminescence enhancing likely due to the intermittent porphyrin π-π stacking. In view of experimental results and theoretical calculations, this distinctive alcohol-vapor-induced luminescence turn-on is attributed to the coordination ability to porphyrin-bound zinc ion, molecular size, and vapor pressure, in which methanol and ethanol are particularly favored.
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BACKGROUND: Chronic intermittent ethanol vapor (CIEV) exposure has been used extensively to produce rodent models of alcohol dependence, but unlike other models of alcohol abuse, CIEV has not been assessed as a model of end-organ damage. The purpose of this study was to characterize the effects of CIEV on peripheral organ systems affected by alcohol abuse, including the liver, lungs, and cardiovascular system. METHODS: Adult male Sprague-Dawley rats were exposed to daily CIEV for a period of 8 weeks (14HR ON/10HR OFF), producing blood alcohol levels of ~200 mg/dl. Controls were exposed to room air. After 8 weeks, echocardiography was performed to assess cardiac function. Indices of liver injury (alanine and aspartate aminotransferases [ALT and AST]; cytochrome p450 2E1 [CYP2E1]; alcohol dehydrogenase [ADH]; Oil Red O and triglyceride content; lipid peroxidation; inflammatory cytokine expression; and macrophage infiltration), and lung inflammatory cell count, proinflammatory cytokine expression, and lipid peroxidation were measured. RESULTS: Left ventricular posterior wall thickness was significantly decreased, and systolic blood pressure was significantly elevated by CIEV compared with air controls. CIEV led to a significant increase in plasma ALT and triglycerides compared with room air controls. CIEV did not affect liver triglyceride content, lipid staining or peroxidation, but increased CYP2E1 and chemokine (C-C motif) ligand 2 (CCL2) protein expression, while decreasing ADH expression. CIEV significantly increased numbers of both polymorphonuclear neutrophils and lymphocytes in the bronchoalveolar lavage fluid, indicative of pulmonary inflammation. However, CIEV did not produce significant changes in lung mass, pulmonary lipid peroxidation, inflammatory cytokine expression, or edema. CONCLUSIONS: These results show that CIEV produces hepatic, pulmonary, and cardiovascular effects in rats similar to those found in other models of chronic alcohol administration. Alcohol vapor administration is a novel method of alcohol-induced tissue injury with high potential for widespread use in alcohol toxicology research.