Activation of ventral tegmental area dopaminergic neurons reverses pathological allodynia resulting from nerve injury or bone cancer
Author
Watanabe, MoeNarita, Michiko
Hamada, Yusuke
Yamashita, Akira
Tamura, Hideki
Ikegami, Daigo
Kondo, Takashige
Shinzato, Tatsuto
Shimizu, Takatsune
Fukuchi, Yumi
Muto, Akihiro
Okano, Hideyuki
Yamanaka, Akihiro
Tawfik, Vivianne L
Kuzumaki, Naoko
Navratilova, Edita
Porreca, Frank
Narita, Minoru
Affiliation
Univ Arizona, Arizona Hlth Sci Ctr, Dept PharmacolIssue Date
2018-01-22
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SAGE PUBLICATIONS INCCitation
Activation of ventral tegmental area dopaminergic neurons reverses pathological allodynia resulting from nerve injury or bone cancer 2018, 14:174480691875640 Molecular PainJournal
Molecular PainRights
© The Author(s) 2018. Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Chronic pain induced by nerve damage due to trauma or invasion of cancer to the bone elicits severe ongoing pain as well as hyperalgesia and allodynia likely reflecting adaptive changes within central circuits that amplify nociceptive signals. The present study explored the possible contribution of the mesolimbic dopaminergic circuit in promoting allodynia related to neuropathic and cancer pain. Mice with ligation of the sciatic nerve or treated with intrafemoral osteosarcoma cells showed allodynia to a thermal stimulus applied to the paw on the injured side. Patch clamp electrophysiology revealed that the intrinsic neuronal excitability of ventral tegmental area (VTA) dopamine neurons projecting to the nucleus accumbens (N.Acc.) was significantly reduced in those mice. We used tyrosine hydroxylase (TH)-cre mice that were microinjected with adeno-associated virus (AAV) to express channelrhodopsin-2 (ChR2) to allow optogenetic stimulation of VTA dopaminergic neurons in the VTA or in their N.Acc. terminals. Optogenetic activation of these cells produced a significant but transient anti-allodynic effect in nerve injured or tumor-bearing mice without increasing response thresholds to thermal stimulation in sham-operated animals. Suppressed activity of mesolimbic dopaminergic neurons is likely to contribute to decreased inhibition of N.Acc. output neurons and to neuropathic or cancer pain-induced allodynia suggesting strategies for modulation of pathological pain states.Note
Open access journal.ISSN
1744-80691744-8069
PubMed ID
29357732Version
Final published versionSponsors
MEXT-Supported Program for the Strategic Research Foundation at Private Universities [S1411019]; JSPS [26293346]Additional Links
http://journals.sagepub.com/doi/10.1177/1744806918756406ae974a485f413a2113503eed53cd6c53
10.1177/1744806918756406
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Except where otherwise noted, this item's license is described as © The Author(s) 2018. Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License.
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