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Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal.
Proinflammatory cytokines signal infection Proinflammatory cytokines are produced locally when pathogens are detected by innate immune cells such as monocytes, or the glial cells that embed nerve and brain cells.
Physiological symptoms include oxidative neuron damage, glial overactivation, and overstimulation of the neuroinflammatory response (6).
Attenuation of cochlear damage from noise trauma by an iron chelator, a free radical scavenger and glial cell line-derived neurotrophic factor in vivo.
A cascade of host responses which terminates in the destruction of axonal Myelin, and entire brain neural and glial elements produces Multiple sclerosis.
It is still possible that other factors contribute to SN hyperechogenicity such as abnormal iron-protein bindings, gliosis, and structural changes of neurons or glial cells (atrophy, morphologic changes of cells) in the SN .