Mice, like humans, show robust individual differences in their sensitivity to pain, pain inhibition, and susceptibility to chronic pain development after injury. Like all biological traits, some proportion of this variability is due to inherited genetic factors ("nature"), some proportion is due to environmental factors ("nurture"), and some proportion is due to the interaction of the two. The identification of the genes responsible for variability in pain traits is accomplished by quantitative trait locus (QTL) mapping followed by some combination of candidate gene testing and/or positional refinement of the QTL region. It's important to note that these "pain variability genes" represent a subset of all "pain genes," defined simply as genes coding for proteins of relevance to pain. The latter type of pain gene can be identified via conventional techniques, transgenic knockout experiments, and microarray gene expression profiling. A compilation of pain genes as defined by transgenic knockout experiments is provided in the Resources (Pain Genes Db) section of this website

Using these techniques, the Pain Genetics Lab and collaborators have provided published evidence for the following genomic regions (and genes) associated with variability in pain.




Likely Gene

Hot Plate Test

Chr. 4, 70 cM


Oprd1 (delta-opioid receptor)

Formalin Test

Chr. 9, 60 cM


Atp1b3 (beta-3 subunit of the sodium-potassium pump)


Chr. 14, 33 Mb


Mapk8 (mitogen-activated protein kinase 8)


Chr.10, 70 cM


Avpr1a (vasopressin receptor 1A)

Paw-Withdrawal Test

Chr. 7, 55 cM


Calca (CGRP)


Chr. 4, 80 Mb


Tyrp1 (tyrosinase-related protein 1)

Spared Nerve Injury

Chr. 5, 123 Mb


P2rx7 (purinergic P2X7 receptor)

Morphine Analgesia

Chr. 1, 10 cM

Female Only



Chr. 9, 20 cM

Female Only



Chr. 9, 40 cM


Htr1b (5-HT receptor,1B)


Chr. 10, 10 cM


Oprm1 (mu-opioid receptor)

U50,488 (kappa-opioid)

Chr. 8, 65 cM

Female Only

Mc1r (melanocortin-1 receptor

Multiple Analgesic Classes

Chr. 1, 95 cM


Kcnj9 (GIRK3; Kir3.3)


The Pain Genetics Lab continues to work towards the identification of genomic regions associated with variability in pain-related traits, and in the identification of the responsible genes within these regions. Current projects are focused on genes relevant to mechanical allodynia after nerve injury and chronic inflammation. In addition to our QTL mapping efforts, much can be learned about pain by examining genetic correlations among pain-related traits. We have tested a common set of 12 inbred mouse strains (all genetically identical "clones" of each other) for many, many types of pain, analgesia, and related traits (including tolerance, dependence, itch). Traits in which the same strains are sensitive and resistant are traits in which variability is mediated by common genes, and thus common physiology. We have used genetic correlation analysis to define primary or fundamental types of pain, to infer the existence of "master" analgesia genes, and to demonstrate that the potency of analgesics in mice is dependent on the type of pain being inhibited.

The vast majority of biomedical research in mice is performed in inbred strains (especially C57BL/6), despite their well-known health problems and low fecundity due to inbreeding depression. This questionable decision is often defended on the basis of the presumed decreased variability of inbred strains (i.e., Ve only) compared to outbred strains (Ve + Vg + Vexg). We conducted a meta-analysis (read it here) comparing the variance of inbred and outbred mice in all papers we could find in which they were tested at the same time for the same trait and reported on the same graph. We find NO difference in trait variability between inbred and outbred mice, and strongly suggest that standard biomedical research studies should be performed in outbred strains or, even better, Diversity Outbred mice.


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Department of Psychology 
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