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Behavioral Genetics of Addiction
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Behavioral Genetics of Addiction

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (19 February 2022) | Viewed by 6687

Special Issue Editor

Dr. Ainhoa Bilbao

E-Mail Website
Guest Editor
1. Animal Facility and Animal Experimentation Unit, Biocruces Bizkaia Health Reseach Institute, 48903 Barakaldo, Spain
2. Central Institute of Mental Health, Faculty of Medicine Mannheim, University of Heidelberg, 68159 Mannheim, Germany
Interests: reward learning; mental health; addictions; behavioral genetics; cannabinoid system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The implementation of genetic approaches into the research field of addiction and substance use disorders has greatly improved the understanding of the mechanisms underlying addiction and addictive behaviors.

This Special Issue of the Journal of Personalized Medicine aims to highlight current progress in the field of the behavioral genetics of addiction by presenting the latest findings obtained from a variety of study designs. These studies will cover research work from both preclinical and clinical levels including, for example, transgenic rodent models, genetically selected rat/mice strains, or human populations using pharmacological, behavioral, or epigenetic approaches.

The scientific advances in the field of behavioral genetics of addiction presented here support a personalized medicine approach to addiction treatments and pharmacotherapies that takes gene-dependent phenotypes into account.

Dr. Ainhoa Bilbao
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • addiction
  • substance use disorders
  • phenotype
  • behavioral models
  • humans
  • rodents
  • genetics
  • pharmacology

Published Papers (3 papers)

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Research

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12 pages, 1402 KiB  
Article
Epigenetic Signatures of Smoking in Five Brain Regions
by Lea Zillich, Eric Poisel, Fabian Streit, Josef Frank, Gabriel R. Fries, Jerome C. Foo, Marion M. Friske, Lea Sirignano, Anita C. Hansson, Markus M. Nöthen, Stephanie H. Witt, Consuelo Walss-Bass, Rainer Spanagel and Marcella Rietschel
J. Pers. Med. 2022, 12(4), 566; https://doi.org/10.3390/jpm12040566 - 2 Apr 2022
Cited by 2 | Viewed by 2434
Abstract
(1) Background: Epigenome-wide association studies (EWAS) in peripheral blood have repeatedly found associations between tobacco smoking and aberrant DNA methylation (DNAm), but little is known about DNAm signatures of smoking in the human brain, which may contribute to the pathophysiology of addictive behavior [...] Read more.
(1) Background: Epigenome-wide association studies (EWAS) in peripheral blood have repeatedly found associations between tobacco smoking and aberrant DNA methylation (DNAm), but little is known about DNAm signatures of smoking in the human brain, which may contribute to the pathophysiology of addictive behavior observed in chronic smokers. (2) Methods: We investigated the similarity of DNAm signatures in matched blood and postmortem brain samples (n = 10). In addition, we performed EWASs in five brain regions belonging to the neurocircuitry of addiction: anterior cingulate cortex (ACC), Brodmann Area 9, caudate nucleus, putamen, and ventral striatum (n = 38–72). (3) Results: cg15925993 within the LOC339975 gene was epigenome-wide significant in the ACC. Of 16 identified differentially methylated regions, two (PRSS50 and LINC00612/A2M-AS1) overlapped between multiple brain regions. Functional enrichment was detected for biological processes related to neuronal development, inflammatory signaling and immune cell migration. Additionally, our results indicate the association of the well-known AHRR CpG site cg05575921 with smoking in the brain. (4) Conclusion: The present study provides further evidence of the strong relationship between aberrant DNAm and smoking. Full article
(This article belongs to the Special Issue Behavioral Genetics of Addiction)
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17 pages, 3055 KiB  
Article
NLRP3 Inflammasome Is Involved in Cocaine-Mediated Potentiation on Behavioral Changes in CX3CR1-Deficient Mice
by Ming-Lei Guo, Ernest T. Chivero, Shannon E. Callen and Shilpa Buch
J. Pers. Med. 2021, 11(10), 963; https://doi.org/10.3390/jpm11100963 - 27 Sep 2021
Cited by 5 | Viewed by 2074
Abstract
Microglia, the primary immunocompetent cells of the brain, are suggested to play a role in the development of drug addiction. Previous studies have identified the microglia-derived pro-inflammatory factor IL1β can promote the progression of cocaine addiction. Additionally, the activation status of microglia and [...] Read more.
Microglia, the primary immunocompetent cells of the brain, are suggested to play a role in the development of drug addiction. Previous studies have identified the microglia-derived pro-inflammatory factor IL1β can promote the progression of cocaine addiction. Additionally, the activation status of microglia and “two-hit hypothesis” have been proposed in the field of drug addiction to explain how early life stress (ELS) could significantly increase the incidence of drug addiction in later life. However, the mechanisms underlying microglia prime and full activation and their roles in drug addiction remain greatly unexplored. Here, we employed CX3CR1-GFP mice (CX3CR1 functional deficiency, CX3CR1−/−) to explore whether primed microglia could potentiate cocaine-mediated behavioral changes and the possible underlying mechanisms. CX3CR1−/− mice revealed higher hyperlocomotion activity and conditional place preference than wild-type (WT) mice did under cocaine administration. In parallel, CX3CR1−/− mice showed higher activity of NLR family pyrin domain-containing 3 (NLRP3) inflammasome than WT mice. Interestingly, CX3CR1 deficiency itself could prime NLRP3 signaling by increasing the expression of NLPR3 and affect lysosome biogenesis under basal conditions. Taken together, our findings demonstrated that the functional status of microglia could have an impact on cocaine-mediated reward effects, and NLRP3 inflammasome activity was associated with this phenomenon. This study was consistent with the two-hit hypothesis and provided solid evidence to support the involvement of microglia in drug addiction. Targeting the NLRP3 inflammasome may represent a novel therapeutic approach for ameliorating or blocking the development of drug addiction. Full article
(This article belongs to the Special Issue Behavioral Genetics of Addiction)
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8 pages, 646 KiB  
Brief Report
Melatonin Reduces Alcohol Drinking in Rats with Disrupted Function of the Serotonergic System
by Ieva Poceviciute, Rokas Buisas, Osvaldas Ruksenas and Valentina Vengeliene
J. Pers. Med. 2022, 12(3), 355; https://doi.org/10.3390/jpm12030355 - 26 Feb 2022
Viewed by 1600
Abstract
The reason for the limited treatment success of substance-use-related problems may be a causal heterogeneity of this disorder that, at least partly, is manifested as differences in substance-use motives between individuals. The aim of the present study was to assess if rats with [...] Read more.
The reason for the limited treatment success of substance-use-related problems may be a causal heterogeneity of this disorder that, at least partly, is manifested as differences in substance-use motives between individuals. The aim of the present study was to assess if rats with pharmacologically induced differences in the function of the serotonergic system would respond differently to melatonin treatment compared to control rats with respect to voluntary alcohol consumption. To achieve this goal, we treated rats neonatally with the selective serotonin transporter (SERT) inhibitor escitalopram. This procedure has been reported to cause long-lasting sleep abnormalities in rodents. The study demonstrated that during adulthood, rats that had been treated with escitalopram tended to drink higher amounts of alcohol compared to control rats. Further, administration of melatonin significantly decreased the alcohol intake in escitalopram-treated animals but caused only a slight, nonsignificant reduction in the alcohol consumption by control rats. In conclusion, our data support the therapeutic potential of melatonin as a treatment for alcohol use disorder. However, interindividual differences between alcohol users may considerably modify the outcome of the melatonin treatment, whereby patients that manifest lower sleep quality due to disruption of serotonergic activity are more likely to benefit from this treatment. Full article
(This article belongs to the Special Issue Behavioral Genetics of Addiction)
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