ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms of Addictive Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 2916

Special Issue Editor


E-Mail Website
Guest Editor
Department of Acupuncture, Moxibustion and Acupoint, College of Korean Medicine, Daegu Haany University, Daegu 42158, Republic of Korea
Interests: acupuncture; complementary and alternative medicine; drug addiction; opioid
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Addiction to drugs is one of the most serious health problems worldwide. Although a great amount of research has been performed in recent decades, many aspects remain unknown, and there are large numbers of people suffering from this issue.  Importantly, the progression of drug addiction involves alterations in normal brain circuitry that result in long-lasting drug-induced neuroplastic changes. Critical neurotransmitters (i.e., gamma-aminobutyric acid, glutamate, dopamine, opioid peptides, serotonin, acetylcholine, endocannabinoids, corticotrophin releasing factor) and neurocircuits (i.e., ventral tegmental area, nucleus accumbens, amygdala, cerebellum, prefrontal cortex) underlie the pathological changes at each of these stages. Thus the mechanisms underlying how one becomes addicted to drugs need to be elucidated further and through more diverse approaches, including the molecular pathway. Additionally, many studies on pharmacological or nonpharmacological therapeutics have been shown to be effective during several phases of drug addiction, such as sensitization, self-administration, withdrawal syndrome, craving, and relapse. However, the limitations of their adverse effects and the fact that these scientific mechanisms are not fully understood make us hesitant to use them. In addition, the interaction mechanism through which negative factors such as stress or emotional problems induce or accelerate addiction during each phase cannot be excluded from addiction research. Finally, the scientific approach must examine evidence related not only to functional disorder or unbalance but also structural plasticity to obtain a complete view of the problem. In this Special Issue, we would like to invite any molecular research providing scientific evidence that helps us to better understand drug addiction and the treatments for it.

Dr. Bong Hyo Lee
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • drug addiction
  • abuse
  • mechanism
  • neuroscience
  • receptor

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

19 pages, 2965 KiB  
Article
Cannabinoid Receptor Type 1 Regulates Drug Reward Behavior via Glutamate Decarboxylase 67 Transcription
by Sun Mi Gu, Sowoon Seo, Daejin Park, Sanghyeon Kim, Santosh Lamichhane, Kyoung-Moon Han, Young-Hoon Kim, Sangmin Lee, Jin Tae Hong, Hye Jin Cha and Jaesuk Yun
Int. J. Mol. Sci. 2021, 22(19), 10486; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910486 - 28 Sep 2021
Cited by 2 | Viewed by 2241
Abstract
Interaction of cannabinoid receptor type 1 (CB1) and GABAergic neuronal activity is involved in drug abuse-related behavior. However, its role in drug-dependent Pavlovian conditioning is not well understood. In this study, we aimed to evaluate the effects of a CB1 agonist, JWH-210, on [...] Read more.
Interaction of cannabinoid receptor type 1 (CB1) and GABAergic neuronal activity is involved in drug abuse-related behavior. However, its role in drug-dependent Pavlovian conditioning is not well understood. In this study, we aimed to evaluate the effects of a CB1 agonist, JWH-210, on the development of conditioned place preference (CPP)-induced by methamphetamine (METH). Pretreatment with a synthetic cannabinoid, JWH-210 (CB1 agonist), increased METH-induced CPP score and METH-induced dopamine release in acute striatal slices. Interestingly, CB1 was expressed in glutamate decarboxylase 67 (GAD67) positive cells, and overexpression of CB1 increased GAD67 expression, while CB1 knockdown reduced GAD67 expression in vivo and in vitro. GAD67 is known as an enzyme involved in the synthesis of GABA. CB1 knockdown in the mice striatum increased METH-induced CPP. When GAD67 decreased in the mice striatum, mRNA level of CB1 did not change, suggesting that CB1 can regulate GAD67 expression. GAD67 knockdown in the mouse striatum augmented apomorphine (dopamine receptor D2 agonist)–induced climbing behavior and METH-induced CPP score. Moreover, in the human brain, mRNA level of GAD67 was found to be decreased in drug users. Therefore, we suggest that CB1 potentiates METH-induced CPP through inhibitory GABAergic regulation of dopaminergic neuronal activity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Addictive Disorders)
Show Figures

Figure 1

Back to TopTop