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Grant: Operating Grant

University of Calgary

$882,662.00

Pannexin-1 Channel Opening in Neurons

EF 2013-14

Résumé
In the brain, neurons utilize fast synaptic transmission to communicate with each other. A central component of this intercellular communication are the NMDA type of glutamate receptors, which are also strongly implicated in neuronal death and dysfunction during diseases such as stroke. Much has been learned about how NMDA receptors function. Our work has uncovered a novel pathway utilized by these ubiquitous receptors that is critical for neuronal death and in changing the strength of interneuronal communication. Here we propose to understand the detailed mechanisms of this non-canonical pathway to provide insight into potential new targets for treating brain damage during strokes.
Programme
Operating Grant
Bénéficiaire
Emplacement
Alberta, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
305861
Name
Thompson Roger J
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Molecular & Cellular Neurosciences - B
Projecttitle
Pannexin-1 Channel Opening in Neurons
Programtype2
Operating Grants
Orgnameinp2
University of Calgary
Cihramount2
$882,662
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Behavioural Outcomes; Electrophysiology; Excitotoxicity; Ischemia; Long Term Depression; Nmda Receptor; Pannexin; Protein-Protein Interactions; Stroke; Two Photon Imaging
Abstract
In the brain, neurons utilize fast synaptic transmission to communicate with each other. A central component of this intercellular communication are the NMDA type of glutamate receptors, which are also strongly implicated in neuronal death and dysfunction during diseases such as stroke. Much has been learned about how NMDA receptors function. Our work has uncovered a novel pathway utilized by these ubiquitous receptors that is critical for neuronal death and in changing the strength of interneuronal communication. Here we propose to understand the detailed mechanisms of this non-canonical pathway to provide insight into potential new targets for treating brain damage during strokes.
Competitiondate
201403
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Thompson, Roger J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $882,662~ $0~