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Brain Sciences
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Brain Structural and Functional Correlates of Addiction
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Brain Structural and Functional Correlates of Addiction

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Behavioral Neuroscience".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 1594

Special Issue Editor

Dr. Chella Kamarajan

E-Mail Website
Guest Editor
Department of Psychiatry and Behavioral Sciences, SUNY Downstate Health Sciences University, Brooklyn, NY 11203, USA
Interests: brain electrophysiology (EEG, ERP, ERO); alcohol use disorder (AUD); addiction; neuropsychology; cognitive functions; brain connectivity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Addiction refers to a state characterized by a chronic and compulsive involvement in either using a substance or engaging in a behavior despite adverse consequences. Addiction involves complex interactions among various factors including neural, genetic, psychological, social, and environmental factors. While numerous studies have attempted to elucidate structural and functional correlates of addiction, a comprehensive model explaining the neurobiological and neurocognitive mechanisms underlying addiction is still lacking. This Special Issue will serve as a platform to host a range of articles related to the neural basis of addiction. The goal of this Special Issue is to publish articles from researchers who are engaged in research aimed at understanding the structural and functional correlates of addiction. The Special Issue will prioritize publishing a collection of novel and cutting-edge research articles relevant to this goal. Both human and animal studies that aim to understand brain structural and functional correlations of substance or behavioral addiction are solicited. Studies that use EEG, structural and functional MRI, and other imaging methods are preferred. Neuropsychological, cognitive, and behavioral studies that explore functional aspects of addiction are also welcome for submission. Brain stimulation and neuromodulation studies on addiction, including multimodal studies involving different experimental methods, will also be considered, as will review articles that integrate relevant findings from the literature.

Dr. Chella Kamarajan
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. Brain Sciences 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 2200 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 (SUDs)
  • behavioral addiction
  • EEG
  • brain oscillations
  • MRI
  • brain imaging
  • brain stimulation
  • cognitive function
  • brain networks

Published Papers (2 papers)

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Research

23 pages, 4192 KiB  
Article
Assessing the Influence of Intermittent Alcohol Access on Acrylamide-Induced Neuronal Toxicity in an Experimental Rat Model
by Abdulaziz Arif A. Alshammari, Awyed Batah Almutairi, Minhajul Arfeen, Abdullah Saleh Alkhamiss, Maha A. Aldubayan, Ahmad H. Alhowail and Vasudevan Mani
Brain Sci. 2024, 14(6), 574; https://doi.org/10.3390/brainsci14060574 - 4 Jun 2024
Viewed by 462
Abstract
Tobacco and alcohol have been identified as health risk behaviors associated with significant unfavorable health consequences, ranking within the list of the top ten causes of mortality and disability-adjusted life years (DALY). The combustion of tobacco leads to the formation of acrylamide (ACR), [...] Read more.
Tobacco and alcohol have been identified as health risk behaviors associated with significant unfavorable health consequences, ranking within the list of the top ten causes of mortality and disability-adjusted life years (DALY). The combustion of tobacco leads to the formation of acrylamide (ACR), which is well known for its neurotoxic effects. Similarly, alcohol consumption has also been widely recognized for its neurotoxic effects. Both substances can affect neurons and neuroglia cells through various pathways. This study sought to examine the impacts of co-administration of ACR and intermittent-access ethanol (IAE) consumption over a period of one month. The experimental group received 20 mg/kg of ACR, administered orally, along with IAE of 20% ethanol sessions lasting 24 h, three times per week. The cognitive outcomes were assessed utilizing the elevated plus maze (EPM), which was employed as a means of assessing the capability to learn and remember, the novel object recognition (NOR) test, which was employed to assess recognition memory, and the Y-maze, which was used to explore a new environment and navigate. Additionally, ELISA assays were performed to examine underlying mechanisms, including markers associated with inflammation (NF-κB, PGE2, and TNF-α), apoptosis (Bcl2, Bax, and Caspase-3), and oxidative stress (MDA, catalase, and GSH). These markers were assessed in the brain homogenate as part of the investigation. Furthermore, a histopathological study was conducted. The findings indicated that NF-κB levels increased significantly in the combination of ACR and IAE groups (ACR + IAE) compared to either the ACR-alone or IAE-alone groups. However, parallel changes were observed in TNF-α, PGE2, Bax, Bcl-2, Caspase-3, GSH, and CAT levels when comparing the ACR + IAE group to the ACR-alone group. Comparable alterations were noted between the ACR + IAE treatment and IAE-alone groups in TNF-α, Bcl-2, MDA, GSH, and CAT levels. Moreover, the histopathological analysis revealed significant changes between the ACR + IAE and the ACR- or IAE-alone groups. Regarding memory parameters assessed using tests including EPM, NOR, and Y-maze, considerable changes were observed across all treatment groups as opposed to the control. Surprisingly, there were no notable differences in the NOR and Y-maze tasks between the alone and combination treatment. Further study is necessary to explore the long-term alteration of co-administering ACR and IAE on behavior, memory, and neurotoxicity-related mechanisms, in order to elucidate their combined effects more clearly. Full article
(This article belongs to the Special Issue Brain Structural and Functional Correlates of Addiction)
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15 pages, 2711 KiB  
Article
Abstinence and Fear Experienced during This Period Produce Distinct Cortical and Hippocampal Adaptations in Alcohol-Dependent Rats
by Noah L. Steiner, Dvijen C. Purohit, Casey M. Tiefenthaler and Chitra D. Mandyam
Brain Sci. 2024, 14(5), 431; https://doi.org/10.3390/brainsci14050431 - 26 Apr 2024
Viewed by 820
Abstract
Previous studies demonstrate that ethanol dependence induced by repeating cycles of chronic intermittent ethanol vapor exposure (CIE) followed by protracted abstinence produces significant gray matter damage via myelin dysfunction in the rodent medial prefrontal cortex (mPFC) and alterations in neuronal excitability in the [...] Read more.
Previous studies demonstrate that ethanol dependence induced by repeating cycles of chronic intermittent ethanol vapor exposure (CIE) followed by protracted abstinence produces significant gray matter damage via myelin dysfunction in the rodent medial prefrontal cortex (mPFC) and alterations in neuronal excitability in the mPFC and the dentate gyrus (DG) of the hippocampus. Specifically, abstinence-induced neuroadaptations have been associated with persistent elevated relapse to drinking. The current study evaluated the effects of forced abstinence for 1 day (d), 7 d, 21 d, and 42 d following seven weeks of CIE on synaptic plasticity proteins in the mPFC and DG. Immunoblotting revealed reduced expression of CaMKII in the mPFC and enhanced expression of GABAA and CaMKII in the DG at the 21 d time point, and the expression of the ratio of GluN2A/2B subunits did not change at any of the time points studied. Furthermore, cognitive performance via Pavlovian trace fear conditioning (TFC) was evaluated in 3 d abstinent rats, as this time point is associated with negative affect. In addition, the expression of the ratio of GluN2A/2B subunits and a 3D structural analysis of neurons in the mPFC and DG were evaluated in 3 d abstinent rats. Behavioral analysis revealed faster acquisition of fear responses and reduced retrieval of fear memories in CIE rats compared to controls. TFC produced hyperplasticity of pyramidal neurons in the mPFC under control conditions and this effect was not evident or blunted in abstinent rats. Neurons in the DG were unaltered. TFC enhanced the GluN2A/2B ratio in the mPFC and reduced the ratio in the DG and was not altered by abstinence. These findings indicate that forced abstinence from CIE produces distinct and divergent alterations in plasticity proteins in the mPFC and DG. Fear learning-induced changes in structural plasticity and proteins contributing to it were more profound in the mPFC during forced abstinence. Full article
(This article belongs to the Special Issue Brain Structural and Functional Correlates of Addiction)
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