In the lab, we are interested in understanding how activity can lead to specific structural changes which may be important for learning, and how such changes affect connectivity within neural circuits. While information can be available over our entire lifespan, it is unclear how it is physically encoded, and how the fidelity of neuronal connections is maintained. A guiding principle in the lab is that neuronal structure and function are intimately linked, and we aim to determine how this relationship allows our brains to learn and remember. The focus of the lab is on single neurons, even single spines, to understand the cellular mechanisms that are important for synaptic plasticity, learning, and information storage. We use 2‐photon microscopy to stimulate living spines (through the activation of caged glutamate), and then visualize structural changes (both in size and shape) in response to this stimulation. We look at how newly synthesized proteins contribute to these changes, and how activity at one site can lead to either cooperation or competition at nearby locations. Several neurodevelopmental disorders in humans are characterized by abnormal spine morphology and a high incidence of autism. Therefore, we study animal models of these disorders in order to determine how modulation of neuronal structure and function can lead to cognitive dysfunction. By combining molecular and genetic tools together with imaging and electrophysiological methodologies, we investigate how information is physically stored in the brain.AffiliationsDepartment of Pathology and Cell BiologyTaub Institute for Research on Alzheimer's Disease and the Aging BrainDepartment of NeuroscienceColumbia Translational Neuroscience Initiative
Ghani, M.U., Mesadi, F, Kanık, S.D., Argunşah, A.Ö., Hobbiss, A.F., Israely, I., Ünay, D., Taşdizen, T., Çetin, M. (2016) Dendritic Spine Classification using Shape and Appearance Features based on Two-Photon Microscopy. J Neurosci Methods. S0165-0270(16)30292-8.
Ramiro-Cortés, Y., Hobbiss, A.F., Israely, I. (2013) Synaptic competition in structural plasticity and cognitive function. Philos Trans R Soc Lond B Biol Sci. 369(1633) p. 20130157.
Ramiro-Cortés, Y.R. and Israely, I. (2013). Long lasting protein synthesis- and activity-dependent spine shrinkage and elimination after synaptic depression. PLoS One. Aug 9;8(8).
Govindarajan, A.*, Israely, I.*, Huang S.Y., Tonegawa, S. (2011). The dendritic branch is the preferred integrative unit for protein synthesis-dependent LTP. Neuron, 69:132-146. (*authors contributed equally)
Arikkath, J., Peng, I.F., Ng, Y.G., Israely, I., Liu, X., Ullian, E.M., Reichardt, L.F. (2009). Delta-catenin regulates spine and synapse morphogenesis and function in hippocampal neurons during development. Journal of Neuroscience, 29(17):5435-42.
Arikkath, J., Israely, I., Tao, Y., Mei, L., Liu, X., Reichardt, L.F. (2008). Erbin controls dendritic morphogenesis by regulating localization of delta-catenin. Journal of Neuroscience, 28(28):7047-56.
Israely, I., Costa R.M., Xie, C.W., Silva A.J., Kosik, K., and Liu, X. (2004). Deletion of the neuron-specific protein delta-catenin leads to severe cognitive and synaptic dysfunction. Current Biology, 14(18):1657-63.
Kosik, K.S., Donahue, C.P., Israely, I., Liu, X., Ochiishi, T. (2004). Delta-catenin at the synaptic-adherens junction. Trends in Cell Biology, 15(3):172-8.
Committees , Council, and Professional Society Memberships
Society for Neuroscience, International Society for Neurochemistry
Synaptic plasticity, neuronal structure, dendritic integration, 2-photon imaging, glutamate uncaging, autism, neurodevelopmental disorders