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Major Advisor(s):
Research Description:
Previously, our lab has shown that glial cells in the retina modulate retinal ganglion cell activity by releasing ATP. ATP in the intracellular space is metabolized to adenosine which leads to the hyperpolarization of retinal ganglion cells. Using calcium imaging and whole-cell electrophysiology we have investigated the cellular mechanisms that cause the adenosine-evoked hyperpolarization and consequent altered spiking of retinal ganglion cells. To determine the intracellular mechanisms mediating the adenosine response, we developed a double patch clamp technique. This technique allows us to acquire control recordings from the cell and then later manipulate that cell's intracellular signaling cascades by introducing reagents through a second patch electrode. We have found that there are two adenosine-evoked currents in retinal ganglion cells. One that is mediated by G-protein gated inward rectifying K + channels and another that is mediated by small conductance Ca 2+ -activated K + channels.
Lab Rotations:
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Paulo Kofuji
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Mark Thomas
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Eric Newman
Courses Taken Beyond the Core Courses:
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NSC 5201
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NSC 5202
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PHCL 5110
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PSY 5960
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PSY 5031
Conferences Attended and Presentations:
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Society for Neuroscience Annual Meeting – 2003, 2005, 2006, 2007, 2008
Committee Members:
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Paulo Kofuji (chair)
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Bob Miller
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Dwight Burkhardt
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Eric Newman (advisor)
Selected Publications and Presentations:
Publications:
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Back-Propagation of Dendritic Action Potentials is a Normal Component of the Impulse Generating Mechanism of Retinal Ganglion cells (submitted)
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Adenosine Inhibition of Retinal Ganglion Cells (in preparation)
Abstracts:
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Adenosine evoked hyperpolarization of retinal ganglion cells is mediated by GIRK channel activation (2005 abstract for SfN)
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Back-propagated impulses in retinal ganglion cells (2007 abstract for SfN)
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A1 Receptor activation of SK channels in retinal ganglion cells (2008 abstract for SfN)
Awards and Honors:
Professional Memberships:
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