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. 2019 Jul 19;12:178. doi: 10.3389/fnmol.2019.00178

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Copyright © 2019 Wang, La and Hamill.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic illustrating differential PIEZO1 and PIEZO2 expression in nociceptive and touch labeled lines and their predicted contributions to normal and abnormal pain states (allodynia and hyperalgesia). Touch is mediated by large cell body/thick axon myelinated DRG neurons (Aβ fibers) that express predominately PIEZO2 with minimal expression of PIEZO1. Nociception is mediated by small body/thin axon unmyelinated (C) fibers and thinly myelinated (Aδ) fibers that express PIEZO2 and relatively high levels of PIEZO1. As discussed in the text, hyperalgesia and allodynia are pathological pain states that may arise from crosstalk between the nociceptive and touch lines in addition to possible sensitization of peripheral nerve endings. Different mechanisms may promote this cross talk. One mechanism may occur within the DRG where inflammation, nerve damage and/or elevated neural activity induces gap junction connections (indicated by the electrical resistance symbol) between large and small diameter neurons. Another mechanism may occur within the dorsal horn in which the normal inhibitory synaptic input (indicated by the cross) that suppresses the influence of excitatory inputs on projecting neurons that transmit pain signals to the brain is reduced. In both cases, signals generated by PIEZO2 activation in the “touch line” may also be transmitted to the “nociceptive line” (see text).