- Date and time: February 09, 2017 from 3:30pm-4:30 pm
- Location: 310 Kelly Hall
- Speaker: Joy Sebe, Ph.D.
- Affiliation: Postdoctoral Fellow University of Washington, Seattle
Calcium has a dose dependent role in cellular function serving as both an important signaling molecule and as a cytotoxic agent at low vs. high cytosolic concentrations. Cytoplasmic Ca2+ levels are tightly regulated by ion channels that limit entry, organellar Ca2+ sinks such as the mitochondria and endoplasmic reticulum (ER) that act as buffers, and pumps that extrude Ca2+ from the cell. When Ca2+ homeostasis is disrupted, cytotoxic levels of Ca2+ are thought to cause neuronal damage and trigger cell death in a host of neurological diseases. Using a combination of electrophysiological, molecular biology and in vivo Ca2+ imaging approaches, I am examining two aspects of Ca2+ homeostasis in a larval zebrafish mechanosensory synapse. First, using a combination of genetically encoded Ca2+ indicators targeted to the cytoplasm, mitochondria and ER, I am examining Ca2+ flow across cellular compartments in sensory cells in response to physiological levels of mechanical stimulation. Second, the bulk of my work has examined glutamate receptors that mediate transmission across the mechanosensory hair cell synapse and identified a potential Ca2+ mediated mechanism for excitotoxic damage and neuronal protection. Lastly, I will present my plans to investigate chronic changes in cellular metabolism that are shaped by activity as well as the role of glutamate receptors in sensory coding. The long-term goal of this work is to identify molecular mechanisms that protect cells and circuits from excitotoxic damage thereby conferring resilience during times of stress.
For more information, contact Anne Wailes : email@example.com
Calcium Homeostasis and Glutamatergic Transmission at the Mechanosensory Hair Cell Synapse