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. 2018 Sep 24;127(5):1246–1258. doi: 10.1213/ANE.0000000000003668

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Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Anesthesia Research Society.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Figure 4. — Dexmedetomidine and clonidine. Dexmedetomidine- and clonidine-induced antinociception occur primarily through enhanced inhibitory activity in the descending nociceptive pathways. Sedation induced by dexmedetomidine or clonidine and loss of consciousness induced by dexmedetomidine occur through NE-mediated disinhibition of the POA of the hypothalamus and decreased noradrenergic signaling in the thalamus and cortex. 5HT indicates serotonin; ACh, acetylcholine; DA, dopamine; DR, dorsal raphé; DRG, dorsal root ganglia; GABA_A, γ-aminobutyric acid receptor subtype A; Gal, galanin; His, histamine; ILN, intralaminar nucleus of the thalamus; LC, locus coeruleus; LDT, laterodorsal tegmental area; NE, norepinephrine; PAF, peripheral afferent fiber; PN, projection neuron; POA, preoptic area; PPT, pedunculopontine tegmental area; RVM, rostral ventral medulla; TMN, tuberomammillary nucleus; vPAG, ventral periaqueductal gray.