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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

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Keywords

chronic pain
microglia
astroglia
neuroinflammation
neuroimmune mechanisms
addiction
anxiety
depression
PTSD

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20 pages, 5545 KiB

Open AccessArticle

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 1278

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 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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