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Brain Sciences
Special Issues
Glial and Neuroimmune Mechanisms in Chronic Pain and Comorbid Disorders
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Glial and Neuroimmune Mechanisms in Chronic Pain and Comorbid Disorders

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".

Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 2584

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,

Chronic pain, involving conditions such as neuroinflammatory and neuropathic pain disorders, is highly prevalent but remains poorly understood. Currently, major therapeutic drugs are directed primarily at neurons, even though signaling between glia, immune cells, and neurons is now appreciated as critical for the initiation and maintenance of chronic pain. This special research topic aims to publish breakthrough research findings and highlights recent advances in the understanding of fundamental glial, neuroimmune signaling mechanisms and new therapeutic drug targets in experimental models of chronic pain with comorbid disorders.

We welcome research paper and reviews addressing the following themes:

  • Determining the role of microglia in chronic pain and comorbid disorders;
  • Investigating the role of astroglia in chronic pain and co-morbid disorders;
  • Elucidating the role of neuroimmune mechanisms in chronic pain and co-morbid disorders;
  • Determining the role of neuroinflammatory mechanisms in chronic pain;
  • Describing the role of mesocorticolimbic reward circuits and stress pathways in chronic pain and co-morbid disorders;
  • Examining the sex differences in the neurobiology of chronic pain and co-morbid disorders.

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

  • chronic pain
  • microglia
  • astroglia
  • neuroinflammation
  • neuroimmune mechanisms
  • addiction
  • anxiety
  • depression
  • PTSD

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Published Papers (1 paper)

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Research

20 pages, 5545 KiB  
Article
Glial Glutamate Transporter Modulation Prevents Development of Complete Freund’s Adjuvant-Induced Hyperalgesia and Allodynia in Mice
by Ghallab Alotaibi, Amna Khan, Patrick J. Ronan, Kabirullah Lutfy and Shafiqur Rahman
Brain Sci. 2023, 13(5), 807; https://doi.org/10.3390/brainsci13050807 - 16 May 2023
Cited by 1 | Viewed by 1789
Abstract
Glial glutamate transporter (GLT-1) modulation in the hippocampus and anterior cingulate cortex (ACC) is critically involved in nociceptive pain. The objective of the study was to investigate the effects of 3-[[(2-methylphenyl) methyl] thio]-6-(2-pyridinyl)-pyridazine (LDN-212320), a GLT-1 activator, against microglial activation induced by complete [...] Read more.
Glial glutamate transporter (GLT-1) modulation in the hippocampus and anterior cingulate cortex (ACC) is critically involved in nociceptive pain. The objective of the study was to investigate the effects of 3-[[(2-methylphenyl) methyl] thio]-6-(2-pyridinyl)-pyridazine (LDN-212320), a GLT-1 activator, against microglial activation induced by complete Freund’s adjuvant (CFA) in a mouse model of inflammatory pain. Furthermore, the effects of LDN-212320 on the protein expression of glial markers, such as ionized calcium-binding adaptor molecule 1 (Iba1), cluster of differentiation molecule 11b (CD11b), mitogen-activated protein kinases (p38), astroglial GLT-1, and connexin 43 (CX43), were measured in the hippocampus and ACC following CFA injection using the Western blot analysis and immunofluorescence assay. The effects of LDN-212320 on the pro-inflammatory cytokine interleukin-1β (IL-1β) in the hippocampus and ACC were also assessed using an enzyme-linked immunosorbent assay. Pretreatment with LDN-212320 (20 mg/kg) significantly reduced the CFA-induced tactile allodynia and thermal hyperalgesia. The anti-hyperalgesic and anti-allodynic effects of LDN-212320 were reversed by the GLT-1 antagonist DHK (10 mg/kg). Pretreatment with LDN-212320 significantly reduced CFA-induced microglial Iba1, CD11b, and p38 expression in the hippocampus and ACC. LDN-212320 markedly modulated astroglial GLT-1, CX43, and, IL-1β expression in the hippocampus and ACC. Overall, these results suggest that LDN-212320 prevents CFA-induced allodynia and hyperalgesia by upregulating astroglial GLT-1 and CX43 expression and decreasing microglial activation in the hippocampus and ACC. Therefore, LDN-212320 could be developed as a novel therapeutic drug candidate for chronic inflammatory pain. Full article
(This article belongs to the Special Issue Glial and Neuroimmune Mechanisms in Chronic Pain and Comorbid Disorders)
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