- Brain Awareness Week
Molecular and cellular mechanisms of pain transmission and neurodegeneration.
Research in my laboratory is focused on the Ca2+-dependent regulation of neuronal function in the context of pain signaling, synaptic plasticity and neuronal survival. Ca2+ is a ubiquitous second messenger that controls numerous neuronal functions. Combining the properties of a signaling molecule and an ion that rapidly moves across the plasma membrane during excitation, Ca2+ enables coupling between electrical activity and intracellular signaling events. Multiple Ca2+ targets within neurons differ in their Ca2+ affinity, subcellular distribution and sensitivity to the duration of [Ca2+]i elevation. Accordingly, distinct Ca2+-mediated neuronal responses are encoded and determined by the amplitude, subcellular localization and the length of Ca2+ signal. We are using molecular and genetic approaches combined with patch-clamp recordings and fluorescent microscopy to better understand how Ca2+ signals are generated in the neuronal somata, presynaptic boutons and postsynaptic dendritic spines, and how specific patterns of Ca2+ transients regulate synaptic plasticity, gene expression, excitability of pain-conducting neurons and neuronal survival.. We also use behavioral animal models to further explore in vivo the functional significance of the described processes. Research in my laboratory is supported by three NIH R01 grants: NS054614 (PI: Usachev), NS035563 (PI: Hell; Co-PI: Usachev) and NS056244 (PI: Strack; Co-PI: Usachev).