Pain Control by the Selective Local Ablation of Nociceptive Neurons
Description of Invention:
The vanilloid receptor (VR) is a cation channel predominantly expressed on the peripheral processes and perikarya of nociceptive primary afferent neurons. Previous studies have shown that activation of the peripheral receptors by agonists such as capsaicin from hot peppers, or the much more potent resiniferatoxin, produces acute pain sensation which may be followed by desensitization. These inventors discovered that administration of VR agonists in the vicinity of neuronal cell bodies expressing the VR receptor can actually destroy those cells. To control pain and inflammatory disorders, the present invention provides methods and kits for the selective ablation of pain sensing neurons. For example, the intraganglionic administration of a VR agonist selectively ablates primary afferent nociceptive neurons without impairing other sensory modalities. This invention will greatly enhance the ability to control pain, inflammation and other conditions mediated by nociceptive neurons while sparing mental function and other sensations.
Inventors:
Michael Iadarola and Zoltan Olah (NIDCR)
Patent Status:
DHHS Reference No. E-109-2000/0 --
PCT Application No. PCT/US01/09425 filed 22 Mar 2001, which published as WO 02/076444 on 03 Oct 2002
U.S. Patent Application No. 10/472,874 filed 18 Mar 2004
Relevant Publication:
This research has been described, in part, in Olah et al., "Ligand-induced Dynamic Membrane Changes and Cell Deletion Conferred by Vanilloid Receptor 1", J. Biol. Chem., 276, pp. 11021-11030, 2001.
Portfolios: Internal Medicine Central Nervous System
Central Nervous System -Therapeutics-Psychotherapeutics Internal Medicine-Diagnostics-Other Central Nervous System -Therapeutics Internal Medicine-Diagnostics
For Additional Information Please Contact: Norbert J. Pontzer PhD JD
NIH Office of Technology Transfer
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Email: pontzern@mail.nih.gov
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