1. A role for endothelial NO synthase in LTP revealed by adenovirus-mediated inhibition and rescue
- Author
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Kantor, David B., Lanzrein, Markus, Stary, S. Jennifer, Sandoval, Gisela M., Smith, W. Bryan, Sullivan, Brian M., Davidson, Norman, and Schuman, Erin M.
- Subjects
Drug synergism -- Research -- Physiological aspects ,Nitric oxide -- Physiological aspects -- Research ,Adenoviruses -- Physiological aspects -- Research ,Science and technology ,Physiological aspects ,Research - 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 [Ca.sup.2+] influx and to release NO into the extracellular space during LTP induction., Long-term potentiation, a form of synaptic plasticity, can be inhibited by agents that interfere with the activity of NO synthase (NOS), which suggests that NO serves as a retrograde messenger [...]
- Published
- 1996