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Acute alcohol ingestion has been found to impact visual functions, including eye movement, but its effects on corneal biomechanical properties remain unclear. This study aimed to investigate the influence of acute alcohol consumption on corneal biomechanical properties using optical coherence elastography (OCE). An air-coupled ultrasound transducer induced elastic waves in mice corneas in vivo , and a high-resolution phase-sensitive optical coherence tomography (OCT) system tracked the mechanical waves to quantify the elastic wave speed. In vivo measurements were performed on three groups of age- and gender-matched mice: control, placebo (administered saline), and alcohol (administered ethanol) groups. Longitudinal measurements were conducted over a one-hour period to assess acute temporal changes in wave speeds, which are associated with inherent biomechanical properties of the cornea. The results showed a significant decrease in wave speed for the alcohol group after 10 min of ingestion in comparison to pre-ingestion values (p = 0.0096), whereas the temporal wave speed changes for the placebo group were statistically insignificant (p = 0.076). In contrast, the control group showed no significant changes in elastic wave speed and corneal thickness. Furthermore, a significant difference was observed between the wave speeds of the placebo and alcohol groups at each measurement time point between 10 and 50 min (p < 0.05), though both groups exhibited a similar trend in corneal thickness change. The findings of this study have important implications for clinical assessments and research in corneal disorders, highlighting the potential of OCE as a valuable tool for evaluating such changes. [ABSTRACT FROM AUTHOR]

Background: Acute alcohol consumption triggers release of cytokines, which are immune signaling molecules. Dysregulated cytokine levels are associated with impaired immune function, and peripheral cytokine levels may communicate with the brain to propagate drinking-related behaviors. This exploratory study aims to characterize the peripheral cytokine response to an alcohol challenge in a well-controlled laboratory setting.Methods: Moderate alcohol drinkers (n = 17), abstinent for >5 days, consumed alcohol calibrated to achieve blood concentrations of 120 mg/dL. Serum cytokine levels (IL-6, IL-8, IL-12, IFN-γ, TNF-α) were measured prior to drinking, 6 h after drinking, and 24 h after drinking. Linear mixed models evaluated within-subject differences in cytokine levels over time.Results: The pro-inflammatory chemokine IL-8 significantly increased 6 h after alcohol [F(1,34) = 4.13, p = 0.0002, d' = 0.5]. In contrast, the pro-inflammatory cytokine TNF-α significantly decreased 6 h after alcohol [F(1,34) = -3.07, p = 0.004, d' = 0.3]. No cytokines were significantly different from baseline 24 h after alcohol.Conclusions: In our exploratory data, acute alcohol challenge (120 mg/dL) elicits dynamic changes in the pro-inflammatory molecules IL-8 and TNF-α. The findings help inform the temporal profile of cytokine response to alcohol, and identify IL-8 as a cytokine of interest for future studies of periphery-brain immune communication. [ABSTRACT FROM AUTHOR]

Addiction has been conceptualized as a specific form of memory that appropriates typically adaptive neural mechanisms of learning to produce the progressive spiral of drug-seeking and drug-taking behavior, perpetuating the path to addiction through aberrant processes of drug-related learning and memory. From that perspective, to understand the development of alcohol use disorders, it is critical to identify how a single exposure to alcohol enters into or alters the processes of learning and memory, so that involvement of and changes in neuroplasticity processes responsible for learning and memory can be identified early. This review characterizes the effects produced by acute alcohol intoxication as a function of brain region and memory neurocircuitry. In general, exposure to ethanol doses that produce intoxicating effects causes consistent impairments in learning and memory processes mediated by specific brain circuitry, whereas lower doses either have no effect or produce a facilitation of memory under certain task conditions. Therefore, acute ethanol does not produce a global impairment of learning and memory, and can actually facilitate particular types of memory, perhaps particular types of memory that facilitate the development of excessive alcohol use. In addition, the effects on cognition are dependent on brain region, task demands, dose received, pharmacokinetics, and tolerance. Additionally, we explore the underlying alterations in neurophysiology produced by acute alcohol exposure that help to explain these changes in cognition and highlight future directions for research. Through understanding the impact that acute alcohol intoxication has on cognition, the preliminary changes potentially causing a problematic addiction memory can better be identified. [ABSTRACT FROM AUTHOR]

Abstract Alcohol (ethanol) abuse remains to be a leading cause of medical, including mental, problems throughout the world. Whether alcohol consumption leads to chronic use, and subsequent alcohol dependency and abuse is known to be influenced by the acute effects of this drug. Numerous factors may influence how alcohol administered acutely affects the individual. For example, the mechanisms engaged by drugs of abuse, e.g. cocaine as well as alcohol, have been shown to overlap with those underlying circadian rhythm, and conversely, the effects of these drugs may be dependent upon the time of day of their consumption. To investigate the interaction between circadian rhythm and alcohol, here we employ a simple vertebrate model organism that was previously successfully utilized in other aspects of alcohol research, the zebrafish. We expose zebrafish to alcohol for 20 min in the morning or in the evening, and analyze the effects of this treatment by comparing 1% (vol/vol) alcohol-treated and control (alcohol naive) zebrafish. We record numerous swim path parameters, and report, for the first time, that the time of day of alcohol administration differentially affects certain behavioral parameters, enhancing some while blunting others. Our results suggest a complex interaction between circadian dependent and alcohol engaged mechanisms, findings that represent both practical complications as well as opportunities for understanding how alcohol affects brain function and behavior of vertebrates. Highlights • Zebrafish received acute alcohol exposure in the morning or in the evening. • Numerous swim path parameters were recorded in a novel tank. • For some behaviors a significant time of day × alcohol treatment interaction was found. • This interaction represents complication and opportunities in alcohol research. • The overlap between circadian and drug abuse related mechanisms is discussed. [ABSTRACT FROM AUTHOR]

Acute alcohol-related behavioral disinhibition has been well studied. But whether individual differences in the personality trait sensation seeking affect alcohol-induced behavioral disinhibition remains uncertain. The present study used functional near-infrared spectroscopy (fNIRS) technique and a response inhibition task (i.e., Go/No-Go) to determine the impact of the sensation seeking trait on the relationship between acute alcohol administration and inhibitory control capacity, and further investigate the neural mechanisms underlying this behavioral effect. Twenty-five high-sensation seekers and twenty-six low-sensation seekers were enrolled in this study. These participants attended two sessions: once for alcohol intake (0.5 g/kg) and once for placebo intake (0 g/kg). Our results showed that high-sensation seekers relative to low-sensation seekers showed a significant decrease in inhibition accuracy under alcohol versus the placebo condition. Moreover, reduced prefrontal activity following acute alcohol consumption was more pronounced in high-sensation seekers compared with low-sensation seekers. These findings showed that alcohol-induced behavioral disinhibition was affected by the personality trait sensation seeking and that recruitment of the prefrontal cortex contributed to the observed behavioral effect. • Behavioral and neural measures of alcohol-induced disinhibition. • Alcohol-induced disinhibition was affected by sensation seeking trait. • Recruitment of the prefrontal cortex contributes to the observed behavioral effect. [ABSTRACT FROM AUTHOR]

Alcohol-approach tendencies have been associated with heavy drinking and play a role in the transition to alcohol abuse. Such cognitive biases might predict future alcohol use better under a low dose of alcohol. The aim of this prospective study was to investigate both the magnitude and the predictive power of alcohol-induced changes on approach-avoidance bias and bias-related cortical asymmetries during response preparation across heavy and light drinking adolescents. In heavy drinking adolescents greater approach-related asymmetry index in the beta-band was observed for soft-drink cues compared to alcohol ones and this increase was associated with increase in difficulty to regulate alcohol intake. Earlier findings demonstrated that young heavy drinkers hold both positive and negative implicit alcohol associations, reflecting an ambiguity towards alcohol. The increase in approach related beta-lateralization for soft-drink cues measured in this study may represent a compensatory effort for the weaker S–R mapping (approaching soft drink). The MRAA findings in this study may highlight a mechanism related to overcompensation due to ambivalent attitudes towards drinking in our heavy drinking sample who had greater problems to limit their alcohol intake compared to light drinkers. Moreover, a relatively strong approach soft-drink and weak approach alcohol reaction-time bias after alcohol predicted decreasing drinking; suggesting that the capacity to control the bias under alcohol could be a protective factor. [ABSTRACT FROM AUTHOR]

The zebrafish is emerging as a popular animal model for alcohol (ethanol or EtOH) addiction due to its simplicity and practical advantages. Two phenomena associated with ethanol addiction are the development of tolerance and withdrawal. Using a multi-level approach in the current study, we characterise ethanol tolerance and withdrawal in zebrafish. We first investigate the temporal trajectory of ethanol concentration in the zebrafish brain in response to an acute exposure and during withdrawal. We report that ethanol concentrations approach a steady state within 60 min of exposure to 0.50% and 1.00% v/v ethanol and rapidly decline and return to zero within 60 min following withdrawal from chronic ethanol exposure (0.50% v/v). We characterise the changes associated with ethanol tolerance and withdrawal in zebrafish by focusing on three domains relevant to ethanol addiction: motor patterns, physiological responses (i.e. cortisol levels), and neurochemical alterations. The use of multiple domains of investigation allowed an in-depth analysis of ethanol induced changes in zebrafish. [ABSTRACT FROM AUTHOR]

Highlights: [•] We investigated the preparatory activity related with the alcohol approach bias. [•] Moreover, priming effect of acute alcohol on this bias was tested. [•] Posterior beta-ERD increased during preparation for alcohol-approach trials. [•] Acute alcohol facilitated preparatory processes for approach alcohol trials. [•] EEG studies with the adapted AAT may shed light on approach biases in addiction. [ABSTRACT FROM AUTHOR]

Abstract: Sepsis is a major cause of death worldwide. The associated risks and mortality are known to significantly increase on exposure to alcohol (chronic or acute). The underlying mechanisms of the association of acute ethanol ingestion and poor prognosis of sepsis are largely unknown. The study described here was designed to determine in detail the role of ethanol and TLR4 in the pathogenesis of the sepsis syndrome. The effects of acute ethanol exposure and TLR4 on bacterial clearance, spleen cell numbers, peritoneal macrophage numbers, and cytokine production were evaluated using wild-type and TLR4 hyporesponsive mice treated with ethanol and then challenged with a nonpathogenic strain of Escherichia coli. Ethanol-treated mice exhibited a decreased clearance of bacteria and produced lesser amounts of most pro-inflammatory cytokines in both strains of mice at 2h after challenge. Neither ethanol treatment nor a hyporesponsive TLR4 had significant effects on the cell numbers in the peritoneal cavity and spleen 2h postinfection. The suppressive effect of acute ethanol exposure on cytokine and chemokine production was more pronounced in the wild-type mice, but the untreated hyporesponsive mice produced less of most cytokines than untreated wild-type mice. The major conclusion of this study is that acute ethanol exposure suppresses pro-inflammatory cytokine production and that a hyporesponsive TLR4 (in C3H/HeJ mice) decreases pro-inflammatory cytokine levels, but the cytokines and other mediators induced through other receptors are sufficient to ultimately clear the infection but not enough to induce lethal septic shock. In addition, results reported here demonstrate previously unknown effects of acute ethanol exposure on leukemia inhibitory factor and eotaxin, and provide the first evidence that interleukin (IL)-9 is induced through TLR4 in vivo. [Copyright &y& Elsevier]

Abstract: Extensive evidence indicates that ethanol (alcohol) has immunomodulatory properties. Many of its effects on innate immune response are dose dependent, with acute or moderate use associated with attenuated inflammatory responses, and heavy ethanol consumption linked with augmentation of inflammation. Ethanol may modify innate immunity via functional alterations of the cells of the innate immune system. Mounting evidence indicates that ethanol can diversely affect antigen recognition and intracellular signaling events, which include activation of mitogen activated protein kinases, and NFκB, mediated by Toll-like receptors, leading to altered inflammatory responses. The mechanism(s) underlying these changes may involve dose-dependent effects of ethanol on the fluidity of cell membrane, resulting in interference with the timely assembly or disassembly of lipid rafts. Ethanol could also modify cell activation by specific interactions with cell membrane molecules. [Copyright &y& Elsevier]