PSYC FPX 4310 Assessment 1 Neurobiology of Alcohol Abuse

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Capella University

PSYC FPX 4310 Biological Psychology

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Neurobiology of alcohol abuse

Alcohol is a substance that induces euphoria, reduces anxiety, provides sedation, impairs motor coordination, and affects cognitive functions. It is the oldest known drug of abuse (Garrett & Hough, 2017). Historically, alcohol played a significant cultural role and was integral to various socially sanctioned activities. However, in contemporary times, the controlled social consumption of alcohol has given way to widespread individual abuse. This paper aims to review several scholarly articles on alcohol abuse and summarize key components from these articles.

The Capella library database was utilized to locate relevant articles, using the following search criteria: peer-reviewed, journal articles published after July 17, 2012, with the search terms (Neurobiology) AND (Alcohol abuse). The search was conducted across various databases, given that research on alcohol abuse spans multiple scholarly disciplines.

Article Review

In the following sections, five academic articles will be reviewed and analyzed. The analysis will focus on: 1) the research methods employed in each article, 2) variables related to the hypothesis or alcohol abuse in general, 3) an assessment of how the hypothesis was supported or not and whether the research questions were answered, and 4) a determination and explanation of whether the study was conducted safely and ethically by the authors. This review and analysis will not include any personal opinions or additional interpretations beyond what was reported in the articles.

A mechanism linking two known vulnerability factors for alcohol abuse: Heightened alcohol stimulation and low striatal dopamine D2 receptors (Bocarsly et al., 2019).

This article proposes a connection between alcohol use disorder (AUD) and the reduced expression of striatal dopamine D2 receptors (D2Rs). The research methodology first demonstrates a link between striatal D2Rs and the stimulant effects of ethanol, highlighting the critical role of D2Rs expressed on medium spiny neurons (MSNs) in generating vulnerability. The study offers direct evidence of a mechanism that drives a preference for ethanol and an escalation in drinking. The results were validated using mouse models to study alcohol’s stimulant effects. Finally, the authors show that pre-existing low levels of striatal D2Rs in select cell types are sufficient to modulate ethanol stimulation and alcohol drinking behavior.

The key variables in the study are stimulant and sedative response levels to alcohol and the expression of striatal dopamine D2 in the system.

The study supported the authors’ hypothesis by validating a link between low striatal D2R availability and high sensitivity to the stimulatory effects of ethanol. The study also established that striatal D1R hypersensitivity is the substrate linking these vulnerability factors.

The study was conducted safely and ethically using mice for biological testing.

The neurotransmitters involved in Drosophila alcohol-induced behaviors (Chvilicek et al., 2020).

This article examines the neurobiology of alcohol responses using Drosophila melanogaster (fruit fly) to trace the mechanisms of alcohol action and subsequent effects on behavior. The authors review recent progress in understanding the contribution of seven neurotransmitters to fly behavior, focusing on their roles in alcohol response: dopamine, octopamine, tyramine, serotonin, glutamate, GABA, and acetylcholine.

The key variables include the availability and relevance of current research on the seven neurotransmitters involved in fly behavior combined with alcohol.

Current research demonstrates that alcohol impacts the Drosophila DAergic system, linking many DA-related behaviors to alcohol. Alcohol influences several DA-mediated behaviors in Drosophila, such as locomotion, sedation, and reward.

This study was conducted safely and ethically as it only reviewed other current academic papers on this topic and did not conduct any actual experimentation.Molecular neurobiology of addiction: What’s all the (δ)FosB about? (Ruffle, 2014).This article examines research indicating the molecular changes that accompany addiction. The authors reviewed 126 academic research sources to compile their findings.The key variables were the availability and reliability of the research documentation and the authors’ evaluation of the available research.

The research findings support the authors’ hypothesis that the transcription factor (δ)FosB and associated molecular changes play a significant role in alcohol addiction. (δ)FosB is upregulated in various brain regions following repeated drug exposure and is likely partially responsible for the mechanisms underlying addiction. The genesis of addiction and the accompanying behavioral abnormalities are closely linked to the regulation of gene expression, with genetic changes observed following both acute and chronic drug exposure. These genetic changes are linked to altered levels of transcription factors, including (δ)FOSB, a transcription factor encoded by a gene on human chromosome 19. Further research suggests that understanding (δ)FOSB induction in chronic drug exposure offers a novel approach for evaluating substance addiction profiles.

This study was conducted safely and ethically as it only reviewed other current academic papers on this topic and did not conduct any actual experimentation.Alcohol abuse and cigarette smoking are associated with global DNA hypermethylation: Results from the German investigation on neurobiology in alcoholism (Semmler et al., 2015).This article hypothesizes that alcoholism and chronic alcohol intake in non-addicted subjects may be associated with altered DNA methylation.

The study included 363 consecutive patients referred for hospitalization for alcohol detoxification treatment. Blood samples were obtained on treatment days 1, 3, and 7 to measure global DNA methylation in leukocytes using liquid chromatography tandem mass spectrometry. Genomic DNA was used to genotype seven genetic variants of homocysteine metabolism.The key variables include the degree of alcoholism among the patients, the duration of alcohol addiction, and the number of attempts to undergo detox and rehabilitation.

The results indicate a positive correlation between global DNA methylation and alcohol consumption, suggesting a direct effect of alcohol on DNA methylation, independent of its impact on homocysteine metabolism.This study was conducted ethically on patients already admitted to the hospital for alcohol detoxification. The study received approval from the local ethics committee, and all patients provided informed written consent.Alcohol and nicotine interactions: Pre-clinical models of dependence (Tarren & Bartlett, 2016).This article reviews influential and recent pre-clinical work that is leading the way in modeling the complex relationship between alcohol and nicotine addiction. The authors reviewed 116 research studies, academic articles, and pre-clinical/clinical work focusing on the neuropathology caused by the combination of nicotine and ethanol addiction.

The key variables were the availability and reliability of the research documentation.

The authors’ hypothesis has been validated, as most of the neuroadaptations observed in the reviewed studies were effectively blocked by nicotinic receptor antagonists. This indicates that concurrent alcohol and nicotine use may alter the effectiveness of drugs commonly used to treat individual disorders, suggesting that a combination of treatment options might be more effective for those with multiple dependencies.

This study was conducted safely and ethically as it only reviewed other current academic papers on this topic and did not conduct any actual experimentation.

Conclusion

Alcohol can lead to numerous health and behavioral problems, as evidenced by the approximately 88,000 alcohol-related deaths each year in the United States (Garrett & Hough, 2017). The research highlighted above only begins to address the understanding needed to tackle this significant public health issue. More research on the neurobiology of alcohol and its effects on the human body is necessary to better comprehend and mitigate the complex health and social challenges posed by alcohol abuse.

References

Bocarsly, M. E., da Silva e Silva, D., Kolb, V., Luderman, K. D., Shashikiran, S., Rubinstein, M., Sibley, D. R., Dobbs, L. K., & Alvarez, V. A. (2019). A mechanism linking two known vulnerability factors for alcohol abuse: Heightened alcohol stimulation and low striatal dopamine D2 receptors. Cell Reports, 29(5). https://doi.org/10.1016/j.celrep.2019.09.059

Chvilicek, M. M., Titos, I., & Rothenfluh, A. (2020). The neurotransmitters involved in drosophila alcohol-induced behaviors. Frontiers in Behavioral Neuroscience, 14. https://doi.org/10.3389/fnbeh.2020.607700

Garrett, B., & Hough, G. (2017). Brain & Behavior: An introduction to behavioral neuroscience. SAGE Publications, Inc.

Ruffle, J. K. (2014). Molecular neurobiology of addiction: What’s all the (δ)FosB about? The American Journal of Drug and Alcohol Abuse, 40(6), 428–437. https://doi.org/10.3109/00952990.2014.933840