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Sato D, Narita M, Hamada Y, et al. Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons. Mol Brain. 2022;15(1):10doi: 10.1186/s13041-021-00896-2.
Sato, D., Narita, M., Hamada, Y., Mori, T., Tanaka, K., Tamura, H., Yamanaka, A., Matsui, R., Watanabe, D., Suda, Y., Senba, E., Watanabe, M., Navratilova, E., Porreca, F., Kuzumaki, N., & Narita, M. (2022). Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons. Molecular brain, 15(1), 10. https://doi.org/10.1186/s13041-021-00896-2
Sato, Daisuke, et al. "Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons." Molecular brain vol. 15,1 (2022): 10. doi: https://doi.org/10.1186/s13041-021-00896-2
Sato D, Narita M, Hamada Y, Mori T, Tanaka K, Tamura H, Yamanaka A, Matsui R, Watanabe D, Suda Y, Senba E, Watanabe M, Navratilova E, Porreca F, Kuzumaki N, Narita M. Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons. Mol Brain. 2022 Jan 06;15(1):10. doi: 10.1186/s13041-021-00896-2. PMID: 34991655; PMCID: PMC8740378.
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Mol Brain. 2022 Jan 06;15(1):10. doi: 10.1186/s13041-021-00896-2.

Relief of neuropathic pain by cell-specific manipulation of nucleus accumbens dopamine D1- and D2-receptor-expressing neurons.

Molecular brain

Daisuke Sato, Michiko Narita, Yusuke Hamada, Tomohisa Mori, Kenichi Tanaka, Hideki Tamura, Akihiro Yamanaka, Ryosuke Matsui, Dai Watanabe, Yukari Suda, Emiko Senba, Moe Watanabe, Edita Navratilova, Frank Porreca, Naoko Kuzumaki, Minoru Narita

Affiliations

  1. Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, 142-8501, Tokyo, Japan.
  2. Division of Cancer Pathophysiology, National Cancer Center Research Institute (NCCRI), 5-1-1 Tsukiji, Chuo-ku, 104-0045, Tokyo, Japan.
  3. Department of Molecular and Cellular Medicine, Institute of Medical science, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, 160-0023, Tokyo, Japan.
  4. Institute for Advanced Life Sciences, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, 142-0063, Tokyo, Japan.
  5. Laboratory of Biofunctional Science, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, 142-0063, Tokyo, Japan.
  6. Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, 464-8601, Nagoya, Japan.
  7. Department of Biological Sciences, Graduate school of Medicine, Kyoto University, Yoshida, Sakyo-ku, 606-8501, Kyoto, Japan.
  8. Department of Physical Therapy, Osaka Yukioka College of Health Science, 1-1-41 Sojiji, Ibaraki-City, 567-0801, Osaka, Japan.
  9. Department of Rehabilitation Medicine, Wakayama Medical University, 811-1 Kimiidera,Wakayama City, 641-8509, Wakayama, Japan.
  10. Department of Pharmacology, Arizona Health Sciences Center, University of Arizona, 1501 N. Campbell Avenue, 85724, Tucson, AZ, USA.
  11. Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, 142-8501, Tokyo, Japan. [email protected].
  12. Division of Cancer Pathophysiology, National Cancer Center Research Institute (NCCRI), 5-1-1 Tsukiji, Chuo-ku, 104-0045, Tokyo, Japan. [email protected].
  13. Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, 142-8501, Tokyo, Japan. [email protected].
  14. Division of Cancer Pathophysiology, National Cancer Center Research Institute (NCCRI), 5-1-1 Tsukiji, Chuo-ku, 104-0045, Tokyo, Japan. [email protected].

PMID: 34991655 PMCID: PMC8740378 DOI: 10.1186/s13041-021-00896-2

Abstract

Emerging evidence suggests that the mesolimbic dopaminergic network plays a role in the modulation of pain. As chronic pain conditions are associated with hypodopaminergic tone in the nucleus accumbens (NAc), we evaluated the effects of increasing signaling at dopamine D1/D2-expressing neurons in the NAc neurons in a model of neuropathic pain induced by partial ligation of sciatic nerve. Bilateral microinjection of either the selective D1-receptor (Gs-coupled) agonist Chloro-APB or the selective D2-receptor (Gi-coupled) agonist quinpirole into the NAc partially reversed nerve injury-induced thermal allodynia. Either optical stimulation of D1-receptor-expressing neurons or optical suppression of D2-receptor-expressing neurons in both the inner and outer substructures of the NAc also transiently, but significantly, restored nerve injury-induced allodynia. Under neuropathic pain-like condition, specific facilitation of terminals of D1-receptor-expressing NAc neurons projecting to the VTA revealed a feedforward-like antinociceptive circuit. Additionally, functional suppression of cholinergic interneurons that negatively and positively control the activity of D1- and D2-receptor-expressing neurons, respectively, also transiently elicited anti-allodynic effects in nerve injured animals. These findings suggest that comprehensive activation of D1-receptor-expressing neurons and integrated suppression of D2-receptor-expressing neurons in the NAc may lead to a significant relief of neuropathic pain.

© 2022. The Author(s).

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