Grant: Operating Grant
University of Calgary
$1,027,203.00
Dysregulation of T-type channel trafficking in inflammatory and neuropathic pain
FY 2013-14
Summary
Chronic pain can be a debilitating condition for which there are currently few treatment options, leading to a major burden on our Health care system and the Canadian economy due to lost productivity. We have discovered a previously unrecognized mechanism that contributes to the development of chronic pain states. Upon initiation of a painful stimulus, electrical signals travel along specific nerve cells from the site of the injury to the spinal cord where they communicate with another set of nerve cells that connect to the brain where pain is perceived as an unpleasant sensation. These electrical impulses depend on ion channels, and among these are a group of proteins called T-type calcium channels. When these T-type calcium channels are too active, or if there are too many present in the nerve cells, there is increased pain signalling, and this is exactly what appears to happen in chronic pain conditions. We have discovered how this occurs at the molecular level and we will now build on our exciting preliminary data to learn more about what precisely leads to the greater numbers of T-type calcium channels. We will then use this information to design new ways to interfere with this process, and apply this information to treat pain in mice. We hope that this will ultimately lead to new drug molecules that can be used to treat pain in the human population. This in turn will have a major benefit to society.
Department
Program
Operating Grant
Recipient
Location
Alberta, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
303718
Name
Zamponi Gerald W
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Pharmacology & Toxicology
Projecttitle
Dysregulation of T-type channel trafficking in inflammatory and neuropathic pain
Programtype2
Operating Grants
Orgnameinp2
University of Calgary
Cihramount2
$1,027,203
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Calcium Channels; Cell Signalling; Channel Trafficking; Deubiquitination; Inflammatory Pain; Neuropathic Pain; Ubiquitination
Abstract
Chronic pain can be a debilitating condition for which there are currently few treatment options, leading to a major burden on our Health care system and the Canadian economy due to lost productivity. We have discovered a previously unrecognized mechanism that contributes to the development of chronic pain states. Upon initiation of a painful stimulus, electrical signals travel along specific nerve cells from the site of the injury to the spinal cord where they communicate with another set of nerve cells that connect to the brain where pain is perceived as an unpleasant sensation. These electrical impulses depend on ion channels, and among these are a group of proteins called T-type calcium channels. When these T-type calcium channels are too active, or if there are too many present in the nerve cells, there is increased pain signalling, and this is exactly what appears to happen in chronic pain conditions. We have discovered how this occurs at the molecular level and we will now build on our exciting preliminary data to learn more about what precisely leads to the greater numbers of T-type calcium channels. We will then use this information to design new ways to interfere with this process, and apply this information to treat pain in mice. We hope that this will ultimately lead to new drug molecules that can be used to treat pain in the human population. This in turn will have a major benefit to society.
Competitiondate
201403
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Zamponi, Gerald W
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,027,203~ $0~