Fig. 3
From: Spinal cord stimulation in chronic pain: evidence and theory for mechanisms of action
Mechanisms of Hyperalgesia and Allodynia. Panel a) Non-pathologic nociception whereby C-fiber and Aβ inputs relay through an interneuron to modulate ascending signals via the projection neuron. Panel b) Nerve injury or repeated peripheral c-fiber stimuli leads to central sensitization through multiple mechanisms including changes in receptor kinetics, resting membrane potential and phenotypic transformation of Aβ afferent fibers. Through long term potentiation and altered receptor expression at the post receptor density zone, subthreshold stimulation evokes action potentials leading to classic hyperalgesia. Aβ axon sprouting after injury and secretion of substance P may offer further explanation for the development of tactile allodynia. Acronyms: Glu (Glutamate), Gly (Glycine), GABA (gamma amino butyric acid), SP (Substance P), BDNF (Brain Derived Neurotrophic Factor), CGRP (Calcitonin Gene Related Peptide), MGLUR (metabotropic glutamate receptor), TRKB (Tropomyosin receptor kinase), GABAR (GABA Receptor), AMPAR (AMPA Receptor), CGRPR (CGRP Receptor), NMDAR (NMDA Receptor), NK1R (Neurokinin-1 Receptor), LTP (Long Term Potentiation)