1. A role for endothelial NO synthase in LTP revealed by adenovirus-mediated inhibition and rescue.
- Author
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Kantor DB, Lanzrein M, Stary SJ, Sandoval GM, Smith WB, Sullivan BM, Davidson N, and Schuman EM
- Subjects
- Adenoviridae genetics, Animals, CHO Cells, Cell Membrane enzymology, Cricetinae, Cytosol enzymology, Genetic Vectors, In Vitro Techniques, Mice, Myristic Acid, Myristic Acids metabolism, Myristic Acids pharmacology, Nitric Oxide Synthase genetics, Recombinant Fusion Proteins metabolism, Synaptic Transmission, Transfection, Endothelium enzymology, Hippocampus physiology, Long-Term Potentiation drug effects, Neurons physiology, Nitric Oxide Synthase metabolism
- Abstract
Pharmacological studies support the idea that nitric oxide (NO) serves as a retrograde messenger during long-term potentiation (LTP) in area CA1 of the hippocampus. Mice with a defective form of the gene for neuronal NO synthase (nNOS), however, exhibit normal LTP. The myristoyl protein endothelial NOS (eNOS) is present in the dendrites of CA1 neurons. Recombinant adenovirus vectors containing either a truncated eNOS (a putative dominant negative) or an eNOS fused to a transmembrane protein were used to demonstrate that membrane-targeted eNOS is required for LTP. The membrane localization of eNOS may optimally position the enzyme both to respond to Ca2+ influx and to release NO into the extracellular space during LTP induction.
- Published
- 1996
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