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.

Recent Publications:

Mi, H., H. Haeberle, and B.A. Barres (2001) Endothelial cells induce astrocyte differentiation. J. Neurosci.  2, 1538-47.



Wang, S., A. Sdrulla, G. Weinmaster, and B.A. Barres (2001) Control of oligodendrocyte



differentiation by Id2.   Neuron 29, 603-614.



Kaplan, M., M. Cho, L. Isom, R. Levinson and B. Barres (2001) Differential control of clustering of the sodium channels  Nav1.2 and  Nav1.6 at developing CNS nodes of Ranvier. Neuron 30, 105-119.



Ullian, E., S. Sapperstein, and B.A. Barres (2001) Control of synapse number by glia. Science 291:657-61.



Goldberg, J., J. Espinosa, Y. Xu, N. Davidson, G. Kovacs, and B.A. Barres (2001) CNS axon extension does not occur by default but is stimulated by electrical activity together with neurotrophic factors. Neuron, in press.



Goldberg, J., R. Daneman, Y. Hua, and B.A. Barres (2001) An Irreversible, Neonatal Switch from Axonal to Dendritic Growth in the Developing CNS. Neuron,  submitted.