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Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction.

Publication ,  Journal Article
Mogil, JS; Sorge, RE; LaCroix-Fralish, ML; Smith, SB; Fortin, A; Sotocinal, SG; Ritchie, J; Austin, J-S; Schorscher-Petcu, A; Melmed, K ...
Published in: Nat Neurosci
October 23, 2011

Quantitative trait locus mapping of chemical/inflammatory pain in the mouse identified the Avpr1a gene, which encodes the vasopressin-1A receptor (V1AR), as being responsible for strain-dependent pain sensitivity to formalin and capsaicin. A genetic association study in humans revealed the influence of a single nucleotide polymorphism (rs10877969) in AVPR1A on capsaicin pain levels, but only in male subjects reporting stress at the time of testing. The analgesic efficacy of the vasopressin analog desmopressin revealed a similar interaction between the drug and acute stress, as desmopressin inhibition of capsaicin pain was only observed in nonstressed subjects. Additional experiments in mice confirmed the male-specific interaction of V1AR and stress, leading to the conclusion that vasopressin activates endogenous analgesia mechanisms unless they have already been activated by stress. These findings represent, to the best of our knowledge, the first explicit demonstration of analgesic efficacy depending on the emotional state of the recipient, and illustrate the heuristic power of a bench-to-bedside-to-bench translational strategy.

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Published In

Nat Neurosci

DOI

EISSN

1546-1726

Publication Date

October 23, 2011

Volume

14

Issue

12

Start / End Page

1569 / 1573

Location

United States

Related Subject Headings

  • Vasopressins
  • Stress, Psychological
  • Sex Factors
  • Receptors, Vasopressin
  • Quantitative Trait Loci
  • Polymorphism, Single Nucleotide
  • Pain Threshold
  • Pain Measurement
  • Pain
  • Neurology & Neurosurgery
 

Citation

APA
Chicago
ICMJE
MLA
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Mogil, J. S., Sorge, R. E., LaCroix-Fralish, M. L., Smith, S. B., Fortin, A., Sotocinal, S. G., … Fillingim, R. B. (2011). Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction. Nat Neurosci, 14(12), 1569–1573. https://doi.org/10.1038/nn.2941
Mogil, Jeffrey S., Robert E. Sorge, Michael L. LaCroix-Fralish, Shad B. Smith, Anny Fortin, Susana G. Sotocinal, Jennifer Ritchie, et al. “Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction.Nat Neurosci 14, no. 12 (October 23, 2011): 1569–73. https://doi.org/10.1038/nn.2941.
Mogil JS, Sorge RE, LaCroix-Fralish ML, Smith SB, Fortin A, Sotocinal SG, et al. Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction. Nat Neurosci. 2011 Oct 23;14(12):1569–73.
Mogil, Jeffrey S., et al. “Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction.Nat Neurosci, vol. 14, no. 12, Oct. 2011, pp. 1569–73. Pubmed, doi:10.1038/nn.2941.
Mogil JS, Sorge RE, LaCroix-Fralish ML, Smith SB, Fortin A, Sotocinal SG, Ritchie J, Austin J-S, Schorscher-Petcu A, Melmed K, Czerminski J, Bittong RA, Mokris JB, Neubert JK, Campbell CM, Edwards RR, Campbell JN, Crawley JN, Lariviere WR, Wallace MR, Sternberg WF, Balaban CD, Belfer I, Fillingim RB. Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction. Nat Neurosci. 2011 Oct 23;14(12):1569–1573.

Published In

Nat Neurosci

DOI

EISSN

1546-1726

Publication Date

October 23, 2011

Volume

14

Issue

12

Start / End Page

1569 / 1573

Location

United States

Related Subject Headings

  • Vasopressins
  • Stress, Psychological
  • Sex Factors
  • Receptors, Vasopressin
  • Quantitative Trait Loci
  • Polymorphism, Single Nucleotide
  • Pain Threshold
  • Pain Measurement
  • Pain
  • Neurology & Neurosurgery