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Science 6 December 1996:
Vol. 274. no. 5293, pp. 1744 - 1748
DOI: 10.1126/science.274.5293.1744

Reports

A Role for Endothelial NO Synthase in LTP Revealed by Adenovirus-Mediated Inhibition and Rescue

David B. Kantor, Markus Lanzrein, S. Jennifer Stary, Gisela M. Sandoval, W. Bryan Smith, Brian M. Sullivan, Norman Davidson, Erin M. Schuman *

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.

Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA.
*   To whom correspondence should be addressed. E-mail: schumane{at}cco.caltech.edu


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