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Fig. 6 | Bioelectronic Medicine

Fig. 6

From: Spinal cord stimulation in chronic pain: evidence and theory for mechanisms of action

Fig. 6

Local Glia Modulate Synaptic Transmission After Nerve Injury. Glia are intimately associated with spinal excitatory and inhibitory synapses. The release of cytokines and glial mediators on pre and post-synaptic terminals modulates the activity of that synapse. Cytokines released at glutaminergic excitatory synapses augment transmission while cytokines released at GABAergic and Glycinergic synapses attenuates the signal. The net effect of gliosis and release of glial mediators is an increase in spinal cord pain transmission. Novel modes of SCS may modulate glial activity, thereby enacting their antinociceptive mechanisms through this pathway. Acronyms: Glu (Glutamate), GABA (Gamma Aminobutyric Acid), Gly (Glycine), TNF-α (Tumor Necrosis Factor Alpha), IL-1β (Interleukin 1β), IFN-γ (Interferon Gamma), NMDAR (NMDA Receptor), AMPAR (AMPA Receptor), BDNF (Brain Derived Neurotrophic Factor), GABAR (GABA Receptor), GlyR (Glycine Receptor), PGE2 (Prostaglandin E2)

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