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Adam Granger

In the Nicoll lab, I am interested in studying the molecular mechanism of synaptic plasticity, specifically long-term potentiation (LTP) and long-term depression (LTD). LTP and LTD are opposing processes for strengthening and weakening synaptic transmission, respectively, and are thought to underlie learning and memory in the brain. Both LTP and LTD occur through regulation of the number of synaptic AMPA-type glutamate receptors. Specifically, my research focuses on the role of the cytoplamic tails of AMPA receptorss, and how they effect trafficking basally and during synaptic plasticity. To study this, I have primarily use a single-cell moelcular replacement strategy where all endogenous AMPA receptors are replaced by mutated recombinant receptors. I then use electrophysiological whole-cell and outside-out patch-clamp recordings, either in acute hippocampal slices or organotypic slice cultures to assay AMPA receptor function.

Prior to joining the Nicoll lab at UCSF, I studied mathematics and biology at Kalamazoo College. While there, I worked in the lab of Sheri Holmen studying the use of RNAi as a potential anti-viral strategy by targeting genes necessary for viral replication.

In the future, I would like to expand my research to the function of neural circuits. I am interested in the specific computations that neuronal circuits perform, and how those computations are influenced by the specific connectivity of different neuronal subtypes and the properties of the individual neurons within the circuit.

Link to  C.V.

Publications

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