The role of GRIP1 in synaptic scaling

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dc.contributor.advisor Turrigiano, Gina en_US
dc.contributor.author Lin, Heather
dc.date.accessioned 2015-05-13T19:10:42Z
dc.date.available 2015-05-13T19:10:42Z
dc.date.issued 2015 en_US
dc.identifier.uri http://hdl.handle.net/10192/30510
dc.description.abstract Neural circuits develop based on homeostatic mechanisms that stabilize the excitability of neurons about a set point. “Scaling up” occurs when a cell increases synaptic strength to compensate for decreased network activity. Underlying these adjustments of excitability are changes in synaptic strength, which is mediated by AMPA receptors. In particular, glutamate receptor-interacting protein 1 (GRIP1) is a protein that binds GluR2 subunits and has been shown to be necessary for synaptic scaling. Here we show that during scaling, GRIP1 accumulates at exocyst sites. Furthermore, we demonstrate a method of assessing the reliability of detecting sites of colocalization. Additionally, we determined that during synaptic scaling, the rates of recycling exocytosis are unaffected. We further establish that GRIP1 is required for recycling processes, but not sufficient to drive it. en_US
dc.format.mimetype application/pdf en_US
dc.language English en_US
dc.language.iso eng en_US
dc.publisher Brandeis University en_US
dc.rights Copyright by Heather Lin 2015 en_US
dc.title The role of GRIP1 in synaptic scaling en_US
dc.type Thesis en_US
dc.contributor.department Undergraduate Program in Neuroscience en_US
dc.degree.name BS en_US
dc.degree.level Bachelors en_US
dc.degree.discipline Neuroscience en_US
dc.degree.grantor Brandeis University, College of Arts and Sciences en_US


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