T
Timothy H. Murphy
Researcher at University of British Columbia
Publications - 205
Citations - 18444
Timothy H. Murphy is an academic researcher from University of British Columbia. The author has contributed to research in topics: Excitatory postsynaptic potential & Dendritic spine. The author has an hindex of 68, co-authored 195 publications receiving 16792 citations. Previous affiliations of Timothy H. Murphy include Mount Sinai Hospital & Johns Hopkins University.
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Journal ArticleDOI
Plasticity during stroke recovery: from synapse to behaviour.
Timothy H. Murphy,Dale Corbett +1 more
TL;DR: Evidence from animal models suggests that a time-limited window of neuroplasticity opens following a stroke, during which the greatest gains in recovery occur, and how to optimally engage and modify surviving neuronal networks is studied.
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Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress
TL;DR: Glutamate-induced cytotoxicity in N18-RE-105 cells is due to inhibition of cystine uptake, resulting in lowered glutathione levels leading to oxidative stress and cell death.
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Coordinate Regulation of Glutathione Biosynthesis and Release by Nrf2-Expressing Glia Potently Protects Neurons from Oxidative Stress
Andy Y. Shih,Delinda A. Johnson,Gloria Wong,Andrew D. Kraft,Lei Jiang,Heidi Erb,Jeffrey A. Johnson,Timothy H. Murphy +7 more
TL;DR: It is shown that Nrf2 overexpression can reengineer neurons to express this glial pathway and enhance antioxidant gene expression and protect fully cocultured naive neurons from oxidative glutamate toxicity associated with glutathione (GSH) depletion.
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Oxidative stress induces apoptosis in embryonic cortical neurons.
TL;DR: It is found that glutathione depletion leads to hypercondensation and fragmentation of chromatin into spherical or irregular shapes, a morphologic signature of apoptosis, which suggests that oxidative stress can induce apoptosis in neurons.
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Early increase in extrasynaptic NMDA receptor signaling and expression contributes to phenotype onset in Huntington's disease mice.
Austen J. Milnerwood,Clare M. Gladding,Mahmoud A. Pouladi,Alexandra M. Kaufman,Rochelle M. Hines,Jamie D. Boyd,Rebecca W.Y. Ko,Oana Cristina Vasuta,Rona K. Graham,Michael R. Hayden,Timothy H. Murphy,Lynn A. Raymond +11 more
TL;DR: Elevated extrasynaptic NMDAR activity is demonstrated in an animal model of neurodegenerative disease and a candidate mechanism linking several pathways previously implicated in HD pathogenesis is provided and successful early therapeutic intervention in mice is demonstrated.