The nervous system is an amazing network that underlies how we sense and interact with the world, learn, and make memories. At the heart of these processes are the neurons that communicate using electrical and chemical signals. My lab’s research is generally focused on understanding neuronal signaling and how neuronal signaling adapts to changes in external input to the system. We are interested in how neurons and synapses adapt to changes in global neural activity that can occur during pathological conditions like seizure, stroke, or disease, as well as changes in sensory input that can overload a system. We study how neurons change the expression and function of ion channels and receptors to protect proper signaling. Using Drosophila as a model organism allows us to use a wide variety of tools and approaches, including powerful molecular genetics to manipulate protein expression, function, and localization in vivo, cellular and biochemical techniques, electrophysiology from the intact brain, live reporting systems that track transcriptional and neural activity, to whole animal behavior.
PhD in Neuroscience, Washington University School of Medicine, 1995BA in Molecular Biology, Minor in Mathematics , University of California, San Diego, 1990
Byers N, Hahm, E-T, Tsunoda S: Slo2/KNa Channels in Drosophila Protect Against Spontaneous and Induced Seizure-like Behavior Associated with an Increased Persistent Na+ Current. Journal of Neuroscience 2021; 41(43): 9047-9063Eadaim A, Hahm E-T, Justice ED, Tsunoda S: Cholinergic Synaptic Homeostasis is Tuned by an NFAT-Mediated a7 nAChR-Kv4 Coupled Regulatory System. Cell Reports 2020; 32(10): 108119.Hahm E, Nagaraja R, Waro G, Tsunoda S: Cholinergic Homeostatic Synaptic Plasticity Drives the Progression of Aß-Induced Changes in Neural Activity. Cell Reports 2018; 24: 342-354. Ping Y*, Hahm E*, Waro G*, Song Q, Vo-Ba D, Licursi A, Bao H, Ganoe L, Finch K, Tsunoda S: Linking Aß42-Induced Hyperexcitability to Neurodegeneration, Learning and Motor Deficits, and a Shorter Lifespan in an Alzheimer’s Model. PLoS Genetics 2015; 11(3):e1005025.Ping Y, Tsunoda S: Inactivity-Induced Increase in nAChRs Up-Regulates Shal K+ Channels to Stabilize Synaptic Potentials. Nature Neuroscience 2011; 15(1): 90-97.
NeurobiologySynaptic HomeostasisIon Channel and Receptor RegulationDrosophila Genetics and Physiology