Key result
Double nNOS and eNOS mutation impairs CA1 LTP versus single mutations, suggesting mutual compensation.
Why the study?
The role of nitric oxide synthase isoforms in hippocampal long-term potentiation and their compensatory mechanisms was unclear.
Population
Mice with targeted mutations in nNOS, eNOS, and doubly mutant nNOS-/eNOS- mice
Comparison
Doubly mutant nNOS-/eNOS- mice versus single mutant nNOS- or eNOS- mice
Design
Preclinical genetic mutation study
Authors
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Does not inform clinical practice; leaves open whether nNOS/eNOS compensation extends to human hippocampal function.
Neuronal and endothelial forms of nitric oxide synthase can compensate for each other in hippocampal long-term potentiation, providing genetic evidence for NOS involvement in LTP in the stratum radiatum.
Son et al. (1996) studied this question. Double mutation in nNOS and eNOS (nNOS-/eNOS-) vs. Single mutation (nNOS- or eNOS-) was evaluated on Long-term potentiation (LTP) in stratum radiatum and stratum oriens. LTP in stratum radiatum of CA1 was significantly reduced in doubly mutant mice (nNOS-/eNOS-) compared to single mutants, suggesting neuronal and endothelial forms can compensate for each other.
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