Fox, Philip Douglas, authorTamkun, Michael M., advisorAmberg, Gregory C., committee memberVigh, Jozsef, committee memberTsunoda, Susan, committee memberGarrity, Deborah M., committee member2007-01-032016-01-312014http://hdl.handle.net/10217/88429The voltage-gated K+ channel, Kv2.1, is expressed widely in the mammalian CNS, where it carries the majority of the delayed-rectifier current. The Kv2.1 current facilitates high-frequency action potential firing by promoting the repolarization of the membrane potential and subsequent recovery of voltage-gated Na+ channels from inactivation. Furthermore, Kv2.1 displays a unique cell-surface localization to dense, micron-sized clusters which are sensitive to neuronal insults such as glutamate excitotoxicity. The following dissertation presents original research extending our knowledge of the Kv2.1 K+ channel. The majority of Kv2.1 channels are held in a non-conducting state which is incapable of fluxing K+ in response to membrane potential depolarization. These non-conducting channels tend to localize to the micron-sized clusters which distinguish Kv2.1. Non-conducting, clustered Kv2.1 channels remodel the cortical endoplasmic reticulum (cER) into tight connections with the plasma membrane (PM), likely through a direct interaction. Trafficking of membrane proteins, both exo- and endocytosis are localized to the perimeter of the Kv2.1-induced ER/PM contacts by virtue of remodeling the cER underneath the Kv2.1 clusters. Thus the clustering of Kv2.1 functions to bring protein trafficking and intermembrane signaling together at the neuronal soma.born digitaldoctoral dissertationsengCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.ER/PM junctionstraffickingpotassium channelnon-conductingKv2.1endoplasmic reticulumText