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).

Recent publications