July 22, 1994Science
Endothelial NOS and the Blockade of LTP by NOS Inhibitors in Mice Lacking Neuronal NOS
Key result
In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal and blocked by NOS inhibitors, suggesting eNOS rather than nNOS generates NO within the postsynaptic cell during LTP.
Population
Mice with disrupted neuronal-specific NO synthase (nNOS) gene (nNOS- mice) and wild-type mice
Comparison
NOS inhibitors and weak intensity tetanic… vs Wild-type mice
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Supports NO as retrograde messenger in LTP; leaves open relevance to cardiovascular autonomic regulation.
Structured PICO
P
Population
Mice with disrupted neuronal-specific NO synthase (nNOS) gene (nNOS- mice) and wild-type mice
I
Intervention
NOS inhibitors and weak intensity tetanic stimulation
C
Comparator
Wild-type mice
O
Outcome
Long-term potentiation (LTP) in the CA1 region of the hippocampussurrogate
This study suggests that endothelial NOS (eNOS), rather than neuronal NOS (nNOS), generates nitric oxide within the postsynaptic cell during long-term potentiation in the hippocampus.
Cite This Study
O’Dell et al. (1994) studied Long-term potentiation (LTP) in mice. nNOS gene disruption and NOS inhibitors vs. Wild-type mice was evaluated on Long-term potentiation (LTP) induced by weak intensity tetanic stimulation. In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal and blocked by NOS inhibitors, suggesting eNOS rather than nNOS generates NO within the postsynaptic cell during LTP.