Journal
CURRENT BIOLOGY
Volume 29, Issue 2, Pages 192-+Publisher
CELL PRESS
DOI: 10.1016/j.cub.2018.11.030
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Funding
- Canadian Institutes for Health Research
- Natural Sciences and Engineering Research Council of Canada
- Canadian Pain Society/Pfizer Early Career Investigator Pain Research Grant
- Louise and Alan Edwards Foundation
- Multi-Investigator Research Initiative Award from Brain Canada
- Canada Research Chairs program
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Pain memories are hypothesized to be critically involved in the transition of pain from an acute to a chronic state. To help elucidate the underlying neurobiological mechanisms of pain memory, we developed novel paradigms to study context-dependent pain hypersensitivity in mouse and human subjects, respectively. We find that both mice and people become hypersensitive to acute, thermal nociception when tested in an environment previously associated with an aversive tonic pain experience. This sensitization persisted for at least 24 hr and was only present in males of both species. In mice, context-dependent pain hypersensitivity was abolished by castrating male mice, pharmacological blockade of the hypothalamic-pituitary-adrenal axis, or intracerebral or intrathecal injections of zeta inhibitory peptide (ZIP) known to block atypical protein kinase C (including the protein kinase M zeta isoform). In humans, men, but not women, self-reported higher levels of stress when tested in a room previously associated with tonic pain. These models provide a new, completely translatable means for studying the relationship between memory, pain, and stress.
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