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Glial cells, including SGCs, have long been recognized for their roles in response to neuronal damage and injury. SCGs have specifically been implicated in a new role involving the creation and persistence of chronic pain, which may involve hyperalgesia and other forms of spontaneous pain. [30]
The glia to neuron-ratio in the cerebral cortex is 3.72 (60.84 billion glia (72%); 16.34 billion neurons), while that of the cerebellum is only 0.23 (16.04 billion glia; 69.03 billion neurons). The ratio in the cerebral cortex gray matter is 1.48, with 3.76 for the gray and white matter combined. [ 27 ]
PEA's activity is currently seen as a new inroad in the treatment of neuropathic pain and related disorders based on overactivation of glia and glia-related cells, such as in diabetes and glaucoma. [38] Microglia plays a key role in the winding up phenomenon and central sensitization. [39] [40]
Microglia have been implicated in neuropathic pain. They become activated in response to nerve injury, as demonstrated by several animal models. [30] Activated microglia release substances that excite pain-sensitive neurons, including prostaglandins and reactive oxygen species, through the purinergic signaling mechanisms.
Microglia in rat cerebellar molecular layer in red, stained with antibody to IBA1/AIF1. Bergmann glia processes are shown in green, DNA in blue. Microglial cells are extremely plastic, and undergo a variety of structural changes based on location and system needs. This level of plasticity is required to fulfill the vast variety of functions ...
The key cellular components of the neuroimmune system are glial cells, including astrocytes, microglia, and oligodendrocytes. [1] [2] [5] Unlike other hematopoietic cells of the peripheral immune system, mast cells naturally occur in the brain where they mediate interactions between gut microbes, the immune system, and the central nervous system as part of the microbiota–gut–brain axis.
These factors increase the responsiveness of the dorsal horn pain-projection neurons to ensuing stimuli, termed "spinal sensitization", thus amplifying the pain impulse to the brain. Release of glutamate, substance P, and calcitonin gene-related peptide (CGRP) mediates NMDAR activation (originally silent because it is plugged by Mg2+), thus ...
Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]
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