Ben A. Barres






		Ben A. Barres Title Professor Department Neurobiology Developmental Biology Research Interests Development and function of glia. Email barres@stanford.edu Phone 723-3231 Fax 725-3958 Address Fairchild D235 Mail Code: 5125 Faculty Research Description We are interested in the development and function of glial cells in the mammalian central nervous system. To understand the interactions between neurons and glial cells we have developed methods to highly purify and culture retinal ganglion cells (neurons) as well as the glial cell types they interact with, oligodendrocytes and astrocytes, from the rodent optic nerve. We are using a large variety of methods to address these issues including cell purification by immunopanning, tissue culture, patch clamping, immunohistochemistry and molecular biology. Currently, we are focusing on several questions: (1) What are the cell-cell interactions that control myelination and node of Ranvier formation?, (2) Do glial cells play a role in synapse formation and function?,(3) What are the signals that promote the survival and growth of retinal ganglion cells and can we use this knowledge to promote their survival and regeneration after injury?, (4) How do protoplasmic astrocytes, the main glial cell type in gray matter, develop and what is their function?. We have found evidence of several novel glial signals that induce the onset of myelination, the clustering of axonal sodium channels, the survival and growth of retinal ganglion cells, and the formation of synapses. We are characterizing these processes and are attempting to identify these glial-derived molecules. Kaplan, M., Levinson, S.R., and BA Barres (1997) Soluble oligodendrocyte-derived signals induce regularly-spaced sodium channel clusters along CNS axons. NATURE 386, 724-728. Pfrieger, F. and BA Barres (1997) Glial cells regulate synaptic efficacy. SCIENCE 277, 1684-1687. Wang, S, Sdrulla, A, diSibio, G, Bush, G, Nofziger, D, Hicks, C, Weinmaster, G. and BA Barres (1998) Notch receptor activation inhibits oligodendrocyte differentiation. NEURON 21, 63-75 Meyer-Franke, A, Wilkinson, G., Kruttgen, A., Hu, M., Munro, E., Hanson, M., Reichardt, L., and BA Barres (1998) Depolarization and cAMP recruit TrkB to the plasma membrane of CNSneurons.NEURON 21, 681-693 Shen S, Wiemelt, AP, McMorris, FA, and Barres B (1999) Retinal ganglion cells lose trophic responsiveness after axotomy. NEURON 23, 285-295 Areas of Study Cellular Neurobiology Membrane Excitability Developmental Neuroscience SBRC Ph.D.