NDLI: Nerve growth factor rapidly suppresses basal, NMDA-evoked, and AMPA-evoked nitric oxide synthase activity in rat hippocampus in vivo.

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Nerve growth factor rapidly suppresses basal, NMDA-evoked, and AMPA-evoked nitric oxide synthase activity in rat hippocampus in vivo.

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Nerve growth factor rapidly suppresses basal, NMDA-evoked, and AMPA-evoked nitric oxide synthase activity in rat hippocampus in vivo.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lam, H. H. Bhardwaj, A. O'connell, M. T. Traystman, R. J. Sofroniew, M. V. Hanley, D. F.
Description	Author Affiliation: Lam HH ( Medical Research Council Cambridge Centre for Brain Repair and Department of Anatomy, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 2PY, United Kingdom.);
Abstract	In adult forebrain, nerve growth factor (NGF) influences neuronal maintenance and axon sprouting and is neuroprotective in several injury models through mechanisms that are incompletely understood. Most NGF signaling is thought to occur after internalization and retrograde transport of trkA receptor and be mediated through the nucleus. However, NGF expression in hippocampus is rapidly and sensitively regulated by synaptic activity, suggesting that NGF exerts local effects more dynamically than possible through signaling requiring retrograde transport to distant afferent neurons. Interactions have been reported between NGF and nitric oxide (NO). Because NO affects both neural plasticity and degeneration, and trk receptors can mediate signaling within minutes, we hypothesized that NGF might rapidly modulate NO production. Using in vivo microdialysis we measured conversion of L-[14C]arginine to L-[14C]citrulline as an accurate reflection of NO synthase (NOS) activity in adult rat hippocampus. NGF significantly reduced NOS activity to 61% of basal levels within 20 min of onset of delivery and maintained NOS activity at less than 50% of baseline throughout 3 hr of delivery. This effect did not occur with control protein (cytochrome c) and was not mediated by an effect of NGF on glutamate levels. In addition, simultaneous delivery of NGF prevented significant increases in NOS activity triggered by the glutamate receptor agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). Rapid suppression by NGF of basal and glutamate-stimulated NOS activity may regulate neuromodulatory functions of NO or protect neurons from NO toxicity and suggests a novel mechanism for rapidly mediating functions of NGF and other neurotrophins.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	18
Volume Number	95
Language	English
Publisher	National Academy of Sciences
Publisher Date	1998-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hippocampus Drug Effects N-Methylaspartate Physiology Nerve Growth Factors Pharmacology Nitric Oxide Synthase Metabolism Alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Animals Excitatory Amino Acid Antagonists Enzymology Microdialysis Antagonists & Inhibitors Receptors, Glutamate Recombinant Proteins Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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