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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Visualization of quantal synaptic transmission by dendritic calcium imaging
TL;DR: Calcium imaging of cortical neurons grown in primary culture revealed that the probability of spontaneous activity differed among synapses on the same dendrite, and synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.
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Enhanced NAD(P)H:quinone reductase activity prevents glutamate toxicity produced by oxidative stress.
TL;DR: Induction of quinone reductase activity by treatment with t‐butylhydroquinone reduced glutamate toxicity by up to 80% and dicumarol potentiated the toxic effect of glutamate, indicating a new strategy to combat neurodegenerative disease.
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Synaptic regulation of immediate-early genes in brain
Paul F. Worley,Andrew J. Cole,Timothy H. Murphy,Barbara A. Christy,Yusaku Nakabeppu,Jay M. Baraban +5 more
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COX-2-Derived Prostaglandin E2 Produced by Pyramidal Neurons Contributes to Neurovascular Coupling in the Rodent Cerebral Cortex
Alexandre Lacroix,Xavier Toussay,Eitan Anenberg,Clotilde Lecrux,Nerea Ferreirós,Anastassios Karagiannis,Fabrice Plaisier,Patrick Chausson,Frédéric Jarlier,Sean A. Burgess,Elizabeth M. C. Hillman,Irmgard Tegeder,Timothy H. Murphy,Edith Hamel,Bruno Cauli +14 more
TL;DR: It is shown in rats that NMDA-induced vasodilation and hemodynamic responses evoked by whisker stimulation involve cyclooxygenase-2 (COX-2) activity and activation of the prostaglandin E2 (PgE2) receptors EP2 and EP4 receptors.
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Fine mapping of the spatial relationship between acute ischemia and dendritic structure indicates selective vulnerability of layer V neuron dendritic tufts within single neurons in vivo.
TL;DR: The data suggest that the axonal and dendritic circuitry of neurons located 300 μm outside of an ischemic zone can be relatively free of damage or commitment to cell death suggesting that they may be in an ideal position to contribute to functional recovery.