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J Neurophysiol 82: 3367-3377, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3367-3377
Copyright ©1999 by the American Physiological Society

FGF-2 Potentiates Ca2+-Dependent Inactivation of NMDA Receptor Currents in Hippocampal Neurons

Adam L. Boxer,1,2 Herman Moreno,3 Bernardo Rudy,2,3 and Edward B. Ziff1,2

 1Howard Hughes Medical Institute,  2Department of Biochemistry, and  3Department of Physiology and Neuroscience, New York University Medical Center, New York, New York 10016

Boxer, Adam L., Herman Moreno, Bernardo Rudy, and Edward B. Ziff. FGF-2 Potentiates Ca2+-Dependent Inactivation of NMDA Receptor Currents in Hippocampal Neurons. J. Neurophysiol. 82: 3367-3377, 1999. Peptide growth factors such as the neurotrophins and fibroblast growth factors have potent effects on synaptic transmission, development, and cell survival. We report that chronic (hours) treatment with basic fibroblast growth factor (FGF-2) potentiates Ca2+-dependent N-methyl-D-aspartate (NMDA) receptor inactivation in cultured hippocampal neurons. This effect is specific for the NMDA-subtype of ionotropic glutamate receptor and FGF-2. The potentiated inactivation requires ongoing protein synthesis during growth factor treatment and the activity of protein phosphatase 2B (PP2B or calcineurin) during agonist application. These results suggest a mechanism by which FGF-2 receptor signaling may regulate neuronal survival and synaptic plasticity.




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