| Seq #394 | Saturday, 13 March 2004 | |||||||||||||||||||||||||||
| 12:30 PM-2:30 PM Hawaii Convention Center 316-B, Symposium - Group/Division Sponsored | ||||||||||||||||||||||||||||
| Gene Expression and the Genomics of Pain and Analgesic Drug Actions | ||||||||||||||||||||||||||||
Sponsored by: Neuroscience / TMJ, Pharmacology, Therapeutics, & Toxicology | ||||||||||||||||||||||||||||
| Description: Gene Expression and the Genomics of Pain and Analgesic Drug Actions Despite dramatic advances in the neurosciences and pharmacology, analgesic therapy for the past century has been largely limited to local anesthetics, opioids and aspirin-like drugs (i.e. NSAIDs) with the unique limitations of each class. The number of potential targets for analgesia, however, has grown from the traditional few dozen neurotransmitters and inflammatory mediators that have been studied for decades to include an estimated 10 million single nucleotide polymorphisms (SNPs) in humans. If even only a small percentage of this variability contributes to the inflammatory/pain cascade, neural immune interactions and the development of sensitization over time, this would readily explain the apparent differences in pain mechanisms across various diseases and disorders. Current clinical analgesic trials are based on group responses of relatively homogeneous patient samples in standardized clinical models and neither account for this wide molecular-genetic diversity nor provide a basis for extrapolating to heterogeneous patient populations and the use of drugs across varying diseases. This symposium will review the genetic influences on the perception of acute and chronic pain, the development of sensitization and the pharmacogenomics of analgesic drug actions with an emphasis on data from animal and clinical models relevant to dentistry | ||||||||||||||||||||||||||||
| Chairpersons: R. DIONNE and K. HARGREAVES | ||||||||||||||||||||||||||||
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Back to the IADR/AADR/CADR 82nd General Session (March 10-13, 2004)