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