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Brain Sciences
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Glial Mechanisms in Psychiatric Disorders Focusing on Drug Addiction, Anxiety...
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Glial Mechanisms in Psychiatric Disorders Focusing on Drug Addiction, Anxiety and Depression

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

Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 1683

Special Issue Editors

Prof. Dr. Shafiqur Rahman

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, South Dakota State University, Brookings, SD 57007, USA
Interests: neuropharmacology; drug addiction; major depressive disorder; chronic pain; neuroinflammation; nicotinic receptor
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kabirullah Lutfy

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, CA 91766, USA
Interests: neuropeptides; drug and natural reward; pain; addiction; psychostimulants and other addictive drugs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Psychiatric disorders such as drug addiction, chronic anxiety, and major depressive disorder (MDD) are significant global public health problems. However, effective therapeutics by targeting neuronal mechanisms remain elusive. A growing body of preclinical and clinical evidence suggests that glial mechanisms involving microglia and astrocyte are critical in the pathogenesis of behavior-altering psychiatric disorders. The critical role of glial mechanisms continues to emerge as an important therapeutic target for these psychiatric disorders and more questions remain for further exploration in the development of glial-targeted treatment for addiction, anxiety and MDD.

The aim of the current Special Issue is to present the newly identified roles of glia and highlight the discovery of glial abnormalities in these disorders. Important preclinical and clinical findings suggest the involvement of glial mechanisms, with the idea that glial cells may represent a unique target for the development of novel and effective treatment for these psychiatric disorders.

Authors are invited to submit relevant original research articles and review papers.

Prof. Dr. Shafiqur Rahman
Prof. Dr. Kabirullah Lutfy
Guest Editors

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

  • microglia
  • astrocyte
  • drug addiction
  • anxiety
  • major depressive disorder
  • neuroinflammation
  • cytokine
  • immune mechanisms
  • drugs of abuse
  • neuropeptides

Published Papers (2 papers)

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Research

12 pages, 2033 KiB  
Article
Effects of Hydrocodone Overdose and Ceftriaxone on Astrocytic Glutamate Transporters and Glutamate Receptors, and Associated Signaling in Nucleus Accumbens as well as Locomotor Activity in C57/BL Mice
by Woonyen Wong and Youssef Sari
Brain Sci. 2024, 14(4), 361; https://doi.org/10.3390/brainsci14040361 - 05 Apr 2024
Viewed by 473
Abstract
Chronic opioid treatments dysregulate the glutamatergic system, inducing a hyperglutamatergic state in mesocorticolimbic brain regions. This study investigated the effects of exposure to hydrocodone overdose on locomotor activity, expression of target proteins related to the glutamatergic system, signaling kinases, and neuroinflammatory factors in [...] Read more.
Chronic opioid treatments dysregulate the glutamatergic system, inducing a hyperglutamatergic state in mesocorticolimbic brain regions. This study investigated the effects of exposure to hydrocodone overdose on locomotor activity, expression of target proteins related to the glutamatergic system, signaling kinases, and neuroinflammatory factors in the nucleus accumbens. The locomotor activity of mice was measured using the Comprehensive Laboratory Animal Monitoring System (CLAMS). CLAMS data showed that exposure to hydrocodone overdose increased locomotion activity in mice. This study tested ceftriaxone, known to upregulate major glutamate transporter 1 (GLT-1), in mice exposed to an overdose of hydrocodone. Thus, ceftriaxone normalized hydrocodone-induced hyperlocomotion activity in mice. Furthermore, exposure to hydrocodone overdose downregulated GLT-1, cystine/glutamate antiporter (xCT), and extracellular signal-regulated kinase activity (p-ERK/ERK) expression in the nucleus accumbens. However, exposure to an overdose of hydrocodone increased metabotropic glutamate receptor 5 (mGluR5), neuronal nitric oxide synthase activity (p-nNOS/nNOS), and receptor for advanced glycation end products (RAGE) expression in the nucleus accumbens. Importantly, ceftriaxone treatment attenuated hydrocodone-induced upregulation of mGluR5, p-nNOS/nNOS, and RAGE, as well as hydrocodone-induced downregulation of GLT-1, xCT, and p-ERK/ERK expression. These data demonstrated that exposure to hydrocodone overdose can cause dysregulation of the glutamatergic system, neuroinflammation, hyperlocomotion activity, and the potential therapeutic role of ceftriaxone in attenuating these effects. Full article
(This article belongs to the Special Issue Glial Mechanisms in Psychiatric Disorders Focusing on Drug Addiction, Anxiety and Depression)
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16 pages, 2387 KiB  
Article
The α-7 Nicotinic Receptor Positive Allosteric Modulator Alleviates Lipopolysaccharide Induced Depressive-like Behavior by Regulating Microglial Function, Trophic Factor, and Chloride Transporters in Mice
by Sami Alzarea, Amna Khan, Patrick J. Ronan, Kabirullah Lutfy and Shafiqur Rahman
Brain Sci. 2024, 14(3), 290; https://doi.org/10.3390/brainsci14030290 - 19 Mar 2024
Viewed by 871
Abstract
Neuroinflammation contributes to the pathophysiology of major depressive disorder (MDD) by inducing neuronal excitability via dysregulation of microglial brain-derived neurotrophic factor (BDNF), Na-K-Cl cotransporter-1 (NKCC1), and K-Cl cotransporter-2 (KCC2) due to activation of BDNF-tropomyosin receptor kinase B (TrkB) signaling. Allosteric modulation of α7 [...] Read more.
Neuroinflammation contributes to the pathophysiology of major depressive disorder (MDD) by inducing neuronal excitability via dysregulation of microglial brain-derived neurotrophic factor (BDNF), Na-K-Cl cotransporter-1 (NKCC1), and K-Cl cotransporter-2 (KCC2) due to activation of BDNF-tropomyosin receptor kinase B (TrkB) signaling. Allosteric modulation of α7 nAChRs has not been investigated on BDNF, KCC2, and NKCC1 during LPS-induced depressive-like behavior. Therefore, we examined the effects of PNU120596, an α7 nAChR positive allosteric modulator, on the expression of BDNF, KCC2, and NKCC1 in the hippocampus and prefrontal cortex using Western blot analysis, immunofluorescence assay, and real-time polymerase chain reaction. The effects of ANA12, a TrkB receptor antagonist, on LPS-induced cognitive deficit and depressive-like behaviors were determined using the Y-maze, tail suspension test (TST), and forced swim test (FST). Pharmacological interactions between PNU120596 and ANA12 were also examined. Experiments were conducted in male C57BL/6J mice. LPS administration (1 mg/kg) resulted in increased expression of BDNF and the NKCC1/KCC2 ratio and decreased expression of KCC2 in the hippocampus and prefrontal cortex. PNU120596 pretreatment (4 mg/kg) attenuated the LPS-induced increase in the expression of BDNF and NKCC1/KCC2 ratio and the reduction in KCC2 expression in these brain regions. In addition, ANA12 (0.25 or 0.50 mg/kg) reduced the LPS-induced cognitive deficit and depressive-like behaviors measured by a reduced spontaneous alternation in the Y-maze and increased immobility duration in TST and FST. Coadministration of PNU120596 (1 mg/kg) and ANA12 (0.25 mg/kg) prevented the LPS-induced cognitive deficit and depressive-like behaviors. Overall, PNU120596 prevented the LPS-induced depressive-like behavior by likely decreasing neuronal excitability via targeting microglial α7 nAChR in the hippocampus and prefrontal cortex. Full article
(This article belongs to the Special Issue Glial Mechanisms in Psychiatric Disorders Focusing on Drug Addiction, Anxiety and Depression)
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