Bilal F Shanti1*, Ihsan F Shanti2, Khalil Al-Abbadi3, Ali Al Rjoub4 and Ali Otom5
1Omnia Pain Consultants, Pain Medicine, Phoenix, Arizona, USA
2The American Clinic for Interventional Pain and Spine, Amman, Jordan
3Senior Consultant, Physical Medicine and Neurorehabilitation, Amman, Jordan
4Department of Physical Medicine and Rehabilitation, Al Bashir Hospital, Amman, Jordan
5Royal Specialty Center for Spine and Musculoskeletal disorders, Amman, Jordan
*Corresponding Author: Bilal F Shanti, Omnia Pain Consultants, Pain Medicine, Phoenix, Arizona, USA.
Received: May 24, 2020; Published: May 29, 2020
The current clinical management of neuropathic pain remains a real and big challenge to clinicians.
The last 3 decades have witnessed an explosion of research in the molecular neurobiology of pain. The traditional belief that pain modulation is solely based on peripheral and central pain pathways or based on peripheral pain modulators such as bradykinin, substance P and prostaglandin, is becoming secondary and redefined, albeit still valid. The novel look emphasizes on the role of glial cells (Mainly microglia and astrocytes) in the dorsal horn of the spinal cord, and their intricate communication with neurons. Similarly, the presumed passive physiologic role of glial cells being simply related to housekeeping like supporting, maintaining, repairing, nurturing, and protecting the neurons is becoming a mediocre definition. Glial cells, especially microglia, once activated, are found to orchestrate the initiation of pain processes, whereas astrocytes are responsible for pain maintenance. Once triggered, glial activation causes proliferation, morphological changes, and expression of receptors and markers (e.g. glial fibrillary acidic protein (GFAP)) that lead to the production inflammatory mediators (e.g. tumor necrosis factor-, interleukin-1, interleukin-6 (IL-6), nerve growth factor (NGF)), growth factors (brain-derived growth factor (BDNF) and basic fibroblast growth factor (bFGF)), cytokines and chemokines (e.g. MCP-1, CX3CL1, CCL2, CXCL13, CXCR5). This activation can have severe and deleterious effects on pain symptoms and trigger and maintain a serious pain syndrome. This ambivalent function of glial cell activation is the focus of our review manuscript. We feel it is important to understand these mechanisms as these may shed light on potential novel treatment options of neuroinflammation and neuropathic pain. It is important to understand that we have based our review on research on animals and the same may or may not apply for humans, and we have focused mainly on microglia and astrocytes.
Keywords: Glia; Microglia; Astrocytes; Neuropathic Pain; Pain; Neuroinflammation; Chemokines; Cytokines; Glial Activation
Citation: Bilal F Shanti., et al. “The Ambivalent Role of Glial Cells in Neuroinflammation and Neuropathic Pain”. Acta Scientific Neurology 3.6 (2020): 51-58.
Copyright: © 2020 Bilal F Shanti., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.