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The Pain Genetics Lab is broadly interested in physiological mechanisms mediating the perception and inhibition of pain. Pain is a complex, subjective experience that displays considerable variability compared to other sensory modalities. In some instances and in some people, intensely noxious stimuli are not reported as causing pain, whereas others can experience excruciating pain from light touching of the skin. Some people are highly sensitive to pain relief from placebo administration, while others are insensitive to even high doses of morphine. Following nerve injury, only a small proportion of people go on to develop chronic, neuropathic pain.
Research in the Pain Genetics Lab revolves around a central question: why aren't we all alike in our sensitivity to pain, sensitivity to pain-killing drugs, and susceptibility to developing chronic pain. This interindividual variability is, of course, a result of genetic factors (including biological sex), environmental factors, and the interaction of the two. Thus, the Lab performs studies of Pain Genetics, Sex Differences in Pain and Analgesia, and Environmental Factors Influencing Pain Sensitivity. Our studies are almost exclusively performed in the laboratory mouse, but through ongoing collaborations we test the relevance of our findings in humans as well.
We use a multidisciplinary approach ranging from the molecular level (gene mapping/positional cloning, gene expression assays) to the cellular/systems level (immunohistochemistry, pharmacology) to the behavioural level (characterization of inbred mouse strains and transgenic knock-out mice). Recent experiments have implicated particular genes (e.g., Mc1r, encoding the melanocortin-1 receptor; Calca, encoding the calcitonin gene-related peptide) and particular laboratory environmental factors (e.g., experimenter, order-of-testing, social interaction) in pain and analgesic variability. Of particular interest is the identification of sex-specific genes underlying pain sensitivity and analgesic sensitivity in mice. The laboratory has recently shown that in humans as in mice the two sexes possess qualitatively different neural mechanisms underlying the modulation of pain; much ongoing work is devoted to the characterization of this sex-specific neural circuitry.
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