Susan Tsunoda

Faculty Biomedical Sciences

W317 Az

970-491-3665

About Susan

Our studies over the years have focused on the molecular mechanisms and cellular strategies underlying the trafficking and regulation of ion channels, receptors, and signaling proteins. Much of our work has been dedicated to the study of the voltage-dependent Kv4/Shal K+ channel –its regulation, trafficking, and function. Our more recent studies have revealed that expression and turnover of Kv4/Shal channels are affected in two new contexts: in tuning cholinergic synaptic homeostasis (Ping and Tsunoda, Nature Neuroscience 2012), and in a Drosophila model of Alzheimer’s Disease (AD) (Ping et al, PLoS Genetics 2015). We have presented one of the first demonstrations of synaptic homeostasis in cholinergic neurons. Since cholinergic neurons are well known to undergo changes in activity during both development and multiple pathological conditions, including AD, there is increasing interest in understanding how these changes come about, and how they are related. We have recently shown that Aß42 induces an early increase synaptic activity that is followed by later synaptic inhibition, and that endogenous cholinergic synaptic homeostatic mechanisms underlie this progression (Hahm et al., Cell Reports 2018). Although there is increasing interest in cholinergic mechanisms, cholinergic neurons from mammalian models are well known not to survive well in culture, and this has been an impediment in the field. The Drosophila CNS, therefore, offers a genetically tractable cholinergic system that we can manipulate both in vitro and in vivo. Currently, we are digging deeper into the molecular mechanisms underlying how Kv4 channel expression is dynamically regulated to modulate, and perhaps protect, neuronal function and plasticity in both physiological and disease conditions.

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