Dr. Green's laboratory studies intracellular signaling events triggered by membrane electrical activity in order to regulate neuronal survival, neurite growth, and synaptic plasticity - with a particular focus on the promotion of survival by membrane depolarization. His laboratory has special expertise in the use of neonatal rat spiral (cochlear) ganglion neuron cultures that exhibit robust responses to depolarization. Using molecular genetic approaches to test the involvement of specific signaling pathways in the survival-promoting effect of depolarization, Dr. Green and his team have identified three Ca2+-dependent protein kinase systems that independently and additively promote survival through distinct actions in different cellular compartments. The group is now investigating the functions of the key targets of these protein kinases in neuronal survival, using cultured neurons as well as neurons in vivo. For the latter, the group is developing methods whereby genes can be introduced into cochlear neurons and other cells in vivo, which involves the use of viral vector and transgenic mouse approaches. Additionally, in collaboration with Dr. Michael Dailey, Dr. Green's laboratory is investigating the roles that these kinase systems play in synaptogenesis in the developing brain.
Selected Publications:
Zha, X.-M., S.H. Green, and M.E. Dailey (2005) Regulation of hippocampal synapse remodeling by epileptiform activity. Mol. Cell. Neurosci. 29(4), 494-506.
Hansen, M. R., Roehm, P., Xu, N., and Green, S. H. (2006) Overexpression of Bcl-2 or Bcl-xL prevents spiral ganglion neuron death and inhibits neurite growth. Dev. Neurobiol. 67(3), 316-325.
Alam, S.A., Robinson, B.K., J. Huang, and S.H. Green (2007) Prosurvival and proapoptotic intracellular signaling in rat spiral ganglion neurons in vivo after the loss of hair cells. J. Comp. Neurol. 503(6), 832-52.
Bok, J., J. Huang, Q. Wang, and S.H. Green (2007) CaMKII and CaMKIV mediate divergent prosurvival signaling pathways in response to depolarization in neurons. Mol. Cell. Neurosci., 36(1), 13-26.
