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Regulated Release of BDNF by Cortical Oligodendrocytes is Mediated through Metabotropic Glutamate Receptors and the PLC Pathway

Issa Papiss Bagayogo
B.A., 2000
Hunter College
City University of New York

Thesis Advisor: Cheryl F. Dreyfus, Ph.D.
Graduate Program in Neuroscience

CABM Room 010

Thursday, March 12, 2009
10:00 am


A number of studies suggest that oligodendrocytes (OLGs), the myelinating cells of the central nervous system, are also a source of trophic molecules, such as neurotrophins that may influence survival of proximate neurons. What is less clear is how the release of these molecules may be regulated. My studies investigated effects of BDNF derived from cortical OLGs on proximate neurons as well as regulatory mechanisms mediating BDNF release. I determined that BDNF derived from cortical OLGs increased the numbers of VGLUT1 positive glutamatergic cortical neurons. Furthermore, glutamate acting through metabotropic, and not AMPA/Kainate or NMDA receptors, mediate BDNF secretion. The PLC-pathway is a key mediator of metabotropic actions to release BDNF. Treatment of OLGs with the PLC activator m-3M3FBS induced robust release of BDNF, while inhibitors of the pathway significantly inhibited release. Taken together, my studies suggest that OLG lineage cells release BDNF, a molecule trophic for proximate neurons. BDNF release is regulated by glutamate acting through metabotropic glutamate receptors and the PLC pathway. Thus, glutamate and BDNF may be molecules that support neuron-OLG interactions in the cortex.

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