Research in Dr. Aizenman's laboratory is directed towards investigating cellular signaling processes leading to neuronal cell death and devising novel approaches to neuroprotection, including in the auditory system.
Acute and chronic injurious processes in the brain lead to the activation of signaling cascades that eventually result in the demise of neurons. In Dr. Aizenman's laboratory, cellular pathways leading to cell death are molecularly dissected in order to provide novel therapeutic targets to treat neurodegenerative disorders. This laboratory works on potential common final mediators of cell death signaling events that can be effectively targeted to treat neural disorders. This work is primarily focused on acute neuronal injury, such as stroke, although the results obtained from these studies could have broader applications to more chronic neurodegenerative conditions. Over the last several years, the laboratory has investigated redox and photic regulation of NMDA receptors, excitotoxicity, dopamine oxidation pathways, zinc-mediated neurotoxicity, zinc receptor and epilepsy, and Kv2.1 potassium channel facilitated forms of neuronal apoptosis, among other topics.
Select Recent Publications
Yeh, C.-Y., A.M. Bulas, A. Moutal, J.L. Saloman, K.A. Hartnett, C.T. Anderson, T. Tzounopoulos, D. Sun, R. Khanna and E. Aizenman. Targeting a potassium channel/syntaxin interaction ameliorates cell death in ischemic stroke. Journal of Neuroscience 2017; 37:5648-5658.
Justice, J.A., A.J. Schulien, K. He, K.A. Hartnett, E. Aizenman and N.H. Shah. Disruption of Kv2.1 somato-dendritic clusters prevents the apoptogenic increase of potassium currents. Neuroscience 2017; 354:158-167.
Schulien, A.J., J.A. Justice, R. Di Maio, Z.P. Wills, N.H. Shah and E. Aizenman. Zinc-induced calcium release via ryanodine receptors triggers calcineurin-dependent redistribution of cortical neuronal Kv2.1 K+ channels. Journal of Physiology 2016; 594:2647-2659.
He, K., M.C. MCord, K.A. Hartnett and E. Aizenman. Regulation of pro-apoptotic phosphorylation of Kv2.1 K+ channels. PLoS One 2015; 10(6):e0129498.
McCord, M.C., P.H. Kullmann, K. He, K.A. Hartnett, J.P. Horn, I. Lotan and E. Aizenman. Syntaxin-binding domain of Kv2.1 is essential for the expression of apoptotic K+ currents. Journal of Physiology 2014; 592:3511-3521.
Shah, N.H., A.J. Schulien, K. Clemens, T.D. Aizenman, T.M. Hageman, Z.P. Wills and E. Aizenman. Cyclin E1 regulates Kv2.1 channel phospohorylation and localization in neuronal ischemia. Journal of Neuroscience 2014; 34:4326-4331.
McCord, M.C. and E. Aizenman. Convergent calcium and zinc signaling regulates apoptotic Kv2.1 potassium currents. Proceedings of the National Academy of Sciences (USA) 2013; 110:13988-13993.
Norris, C.A., K. He, M.G. Springer, K.A. Hartnett, J.P. Horn and E. Aizenman. Regulation of neuronal pro-apoptotic potassium currents by the hepatitis C virus non-structural protein 5A. Journal of Neuroscience 2012; 32:8865-70.