FGF-2 Potentiates Ca2+-Dependent Inactivation of NMDA Receptor Currents in Hippocampal Neurons-Reference-Cited by-同舟云学术

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

Published:1999-12-01 Issue:6 Volume:82 Page:3367-3377
ISSN:0022-3077
Container-title:Journal of Neurophysiology
language:en
Short-container-title:Journal of Neurophysiology

Author:

Boxer Adam L.¹²,Moreno Herman³,Rudy Bernardo²³,Ziff Edward B.¹²

Affiliation:

1. Howard Hughes Medical Institute,

2. Department of Biochemistry, and

3. Department of Physiology and Neuroscience, New York University Medical Center, New York, New York 10016

Abstract

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.

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

Link

https://www.physiology.org/doi/pdf/10.1152/jn.1999.82.6.3367

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