Minding Oligodendrocytes in the Perspectives of Neuroinflammation and Neural Regeneration

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

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 3455

Special Issue Editor


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Guest Editor
Pain Neuroimmunobiology Laboratory, Institute of Motricity Sciences, Federal University of Alfenas, Alfenas 37130-001, MG, Brazil
Interests: pain; analgesia; neuroinflammation; neuroimmune response; glial cells; pharmacology; physiology
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Special Issue Information

Dear Colleagues,

The Special Issue intends to present studies that investigate the mechanisms involved in neuroinflammation as well as neural regeneration, both preclinical and clinical, in vivo and in vitro, with a focus on the participation of glial cells (oligodendrocytes, microglia and astrocytes) in this process.

Dr. Giovane S. Galdino
Guest Editor

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Keywords

  • neuroinflammation
  • neural regeneration
  • microglia
  • astrocytes
  • oligodendrocytes

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Published Papers (1 paper)

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Review

11 pages, 761 KiB  
Review
IL-10/β-Endorphin-Mediated Neuroimmune Modulation on Microglia during Antinociception
by Thiago Caetano Andrade Belo, Gabriela Xavier Santos, Bruno Eduardo Gabriel da Silva, Bruno Lopes Gonçalves Rocha, Dennis William Abdala, Larissa Alves Moreira Freire, Fernanda Santos Rocha and Giovane Galdino
Brain Sci. 2023, 13(5), 789; https://doi.org/10.3390/brainsci13050789 - 12 May 2023
Cited by 6 | Viewed by 2963
Abstract
Microglia are glial cells centrally related to pathophysiology and neuroimmunological regulation of pain through microglia–neuron crosstalk mechanisms. In contrast, anti-inflammatory mechanisms guided by immunological effectors such as IL-10 trigger the secretion of analgesic substances, culminating in the differential expression of genes encoding endogenous [...] Read more.
Microglia are glial cells centrally related to pathophysiology and neuroimmunological regulation of pain through microglia–neuron crosstalk mechanisms. In contrast, anti-inflammatory mechanisms guided by immunological effectors such as IL-10 trigger the secretion of analgesic substances, culminating in the differential expression of genes encoding endogenous opioid peptides, especially β-endorphin. Thus, when β-endorphin binds to the µ-opioid receptor, it generates neuronal hyperpolarization, inhibiting nociceptive stimuli. This review aimed to summarize the recent advances in understanding the mechanism by which IL-10/β-endorphin can reduce pain. For this, databases were searched for articles from their inception up until November 2022. Two independent reviewers extracted the data and assessed the methodological quality of the included studies, and seventeen studies were considered eligible for this review. Several studies have demonstrated the impact of IL-10/β-endorphin in reducing pain, where IL-10 can stimulate GLP-1R, GRP40, and α7nAChR receptors, as well as intracellular signaling pathways, such as STAT3, resulting in increased β-endorphin expression and secretion. In addition, molecules such as gabapentinoids, thalidomide, cynandione A, morroniside, lemairamin, and cinobufagin, as well as non-pharmacological treatments such as electroacupuncture, reduce pain through IL-10 mediated mechanisms, reflecting a microglia-dependent β-endorphin differential increase. This process represents a cornerstone in pain neuroimmunology knowledge, and the results obtained by different studies about the theme are presented in this review. Full article
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