Different immune cells mediate mechanical pain hypersensitivity in male and female mice

By R. Sorge, Josiane C. S. Mapplebeck, S. Rosen, S. Beggs, Sarah R Taves, Jessica K. Alexander, Loren J. Martin, J. Austin, S. Sotocinal, Di Chen and 11 more. Nature Neuroscience, 2015

1,244 citations recorded by the source corpus.

A large and rapidly increasing body of evidence indicates that microglia-to-neuron signaling is essential for chronic pain hypersensitivity. Using multiple approaches, we found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypersensitivity using adaptive immune cells, likely T lymphocytes. This sexual dimorphism suggests that male mice cannot be used as proxies for females in pain research.

Subfields: Neurology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/59f215bfd9f856c2a337bba0d0f2339ef2731e68

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Citations in the corpus

• Nociceptor Sensory Neuron-Immune Interactions in Pain and Inflammation (2016, positive): “In male mice, p38 activation in microglia following peripheral inflammation induces their expression of BDNF, which activates and sensitizes postsynaptic neurons to induce mechanical hyperalgesia, while, in female mice, this process is primarily mediated by infiltrating T cells [60,61].”