The Pain Genes Database: An interactive web browser of pain-related transgenic knockout studies

Department of Psychology and Centre for Research on Pain, McGill University, 1205 Dr. Penfield Avenue, Montreal, QC, Canada H3A 1B1.
Pain (Impact Factor: 5.84). 10/2007; 131(1-2):3.e1-4. DOI: 10.1016/j.pain.2007.04.041
Source: PubMed

ABSTRACT The transgenic knockout mouse is one of the most important tools of modern biology, and commonly employed by pain researchers to examine the function of genes of interest. Over 400 papers, at a current rate of >60 papers per year, have been published to date describing a statistically significant behavioral pain "phenotype" resulting from the null mutation of a single gene. The standard literature review format is incapable of providing a sufficiently broad and up-to-date overview of the field. We have therefore constructed the Pain Genes Database, an interactive, web-based data browser designed to allow easy access to and analysis of the published pain-related phenotypes of mutant mice (over 200 different mutants at the date of submission). Manuscripts describing results of pain-relevant knockout studies were identified via Medline search. Manuscripts were included in the database if they described the testing of a spontaneous or genetically engineered mutant mouse with null expression of a single gene on a behavioral assay of acute or tonic nociception, injury- or stimulus-induced hypersensitivity (i.e., allodynia or hyperalgesia), or drug- or stress-induced inhibition of nociception (i.e., analgesia), and reported at least one statistically significant difference between the mutant mice and their simultaneously tested wildtype controls. The database features two levels of exploration, one allowing the identification of genes by name, acronym, genomic position or "summary" phenotype, and the other allowing in-depth browsing, paper-by-paper, of specific phenotypes and test parameters. Links to genetic databases and Medline abstracts are provided for each gene and paper. It is our intention to update the database continually based on weekly Medline searches. This database should provide pain researchers with a useful and easy-to-use tool for the generation of novel hypotheses regarding the roles of genes and their protein products in pain processing and modulation. It can be accessed at (or by visiting and clicking on the "Pain Genes Db" link under "Resources").

  • [Show abstract] [Hide abstract]
    ABSTRACT: There is an increasing recognition of the value in integrating behavioral genomics data across species. The fragmentation of public resources, interoperability, and available representations present challenges due to the array of identifiers used to represent each genome feature. Once data are organized into a coherent collection, they can be integrated using a variety of methods to analyze convergent evidence for the roles of genes in behaviors. is a web-based software system that employs many of these techniques and has been used in the study of complex behavior and addiction. These techniques will be increasingly necessary to understand global patterns emerging from experiments in behavioral genomics.
    International Review of Neurobiology 01/2012; 104:1-24. DOI:10.1016/B978-0-12-398323-7.00001-X · 2.46 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Persistent or chronic pain is tightly associated with various environmental changes and linked to abnormal gene expression within cells processing nociceptive signaling. Epigenetic regulation governs gene expression in response to environmental cues. Recent animal model and clinical studies indicate that epigenetic regulation plays an important role in the development/maintenance of persistent pain and, possibly the transition of acute pain to chronic pain, thus shedding light in a direction for development of new therapeutics for persistent pain.
    Translational Research 01/2014; DOI:10.1016/j.trsl.2014.05.012 · 4.04 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Allodynia, hyperalgesia and spontaneous pain are cardinal sensory signs of neuropathic pain. Clinically, many neuropathic pain patients experience affective-motivational state changes, including reduced familial and social interactions, decreased motivation, anhedonia and depression which are severely debilitating. In earlier studies we have shown that sciatic nerve chronic constriction injury (CCI) disrupts social interactions, sleep-wake-cycle and endocrine function in one third of rats, a subgroup reliably identified six days after injury. CCI consistently produces allodynia and hyperalgesia, the intensity of which was unrelated either to the altered social interactions, sleep-wake-cycle or endocrine changes. This decoupling of the sensory consequences of nerve injury from the affective-motivational changes is reported in both animal experiments and human clinical data. The sensory changes triggered by CCI are mediated primarily by functional changes in the lumbar dorsal horn, however, whether lumbar spinal changes may drive different affective-motivational states has never been considered. In these studies, we used microarrays to identify the unique transcriptomes of rats with altered social behaviours following sciatic CCI to determine whether specific patterns of lumbar spinal adaptations characterised this subgroup. Rats underwent CCI and on the basis of reductions in dominance behaviour in resident-intruder social interactions were categorised as having Pain & Disability, Pain & Transient Disability or Pain alone. We examined the lumbar spinal transcriptomes two and six days after CCI. Fifty-four 'disability-specific' genes were identified. Sixty-five percent were unique to Pain & Disability rats, two-thirds of which were associated with neurotransmission, inflammation and/or cellular stress. In contrast, 40% of genes differentially regulated in rats without disabilities were involved with more general homeostatic processes (cellular structure, transcription or translation). We suggest that these patterns of gene expression lead to either the expression of disability, or to resilience and recovery, by modifying local spinal circuitry at the origin of ascending supraspinal pathways.
    PLoS ONE 04/2015; 10(4):e0124755. DOI:10.1371/journal.pone.0124755 · 3.53 Impact Factor