USU Neuroscience

mschell@usuhs.mil
 
Ph.D., Johns Hopkins University, 1997
 
Calcium signalling to the actin cytoskeleton in dendritic spines
 
Dendritic spines, the tiny postsynaptic compartments that decorate almost all excitatory neurons on mammalian brains, are presumed sites of memory formation and storage. Spines isolate calcium signals of high dynamic range inside microdomains, and this process somehow integrates synaptic input over time scales of milliseconds to seconds. Over much longer timescales, spines change their connectivity, shape, size, and number, and this likely reflects some kind of structural plasticity that underlies long-term memory storage.
 
We are studying on how calcium signals influence spine number and shape through their ability to regulate the actin cytoskeleton. To do this we use primary cultures of hippocampal neurons and we rely heavily on live cell imaging approaches. To visualize the actin cytoskeleton in spines, we focus on the enzyme IP3 3-kinase, which is enriched in spines by virtue of its ability to bind to the sides of actin filaments. IP3 3-kinase itself influences calcium signals in spines because it phosphorylates the second messenger IP3 and thereby turns of the signal to release calcium from intracellular stores. The goal of the research is to reveal the molecular pathways by which synaptic calcium signals influence the activity of proteins that regulate the shape of actin in spines.

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