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. 2021 Jul 5;2:696515. doi: 10.3389/fpain.2021.696515

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Copyright © 2021 Tavares, Costa-Pereira and Martins.

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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Neuropathic pain induces adaptations in the descending modulatory pain systems involved in serotoninergic and noradrenergic (NA) neurochemical control, some of which are mediated by local opioidergic control. Major changes occur at the locus coeruleus (LC), rostral ventromedial medulla (RVM), and medullary dorsal reticular nucleus (DRt) and affect top-down modulation of nociceptive transmission at the superficial dorsal horn (SDH). The figure summarizes the alterations occurring in different pain models, namely, traumatic neuropathic pain (TNP), diabetic neuropathic pain (DNP), and chemotherapy-induced neuropathic pain (CINP). The mechanisms underlying top-down modulation in different neuropathic pain models are discussed in this review. Adapted from Paxinos and Watson [22]. 5-HT, serotonin; 5-HT3R, 5-HT3 receptor; α₂-AR - α₂ adrenoreceptor; DBH, dopamine beta hydroxylase; DOR, delta opioid receptor; DRt, dorsal reticular nucleus; LC, locus coeruleus; MOR, μ-opioid receptor; NA, noradrenergic; NET, noradrenaline transporter; RVM, rostral ventromedial medulla; SDH, superficial dorsal horn; TH, tyrosine hydroxylase; TpH, tryptophan hydroxylase.