Long-term potentiation is reduced in mice that are doubly mutant in endothelial and neuronal nitric oxide synthase

Cell. 1996 Dec 13;87(6):1015-23. doi: 10.1016/s0092-8674(00)81796-1.

Abstract

Nitric oxide (NO) has been implicated in hippocampal long-term potentiation (LTP), but LTP is normal in mice with a targeted mutation in the neuronal form of NO synthase (nNOS-). LTP was also normal in mice with a targeted mutation in endothelial NOS (eNOS-), but LTP in stratum radiatum of CA1 was significantly reduced in doubly mutant mice (nNOS-/eNOS-). By contrast, LTP in stratum oriens was normal in the doubly mutant mice. These results provide the first genetic evidence that NOS is involved in LTP in stratum radiatum and suggest that the neuronal and endothelial forms can compensate for each other in mice with a single mutation. They further suggest that there is also a NOS-independent component of LTP in stratum radiatum and that LTP in stratum oriens is largely NOS independent.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Electrophysiology
  • Endothelium / enzymology
  • Long-Term Potentiation / physiology*
  • Mice
  • Mice, Mutant Strains
  • Mutagenesis / physiology
  • Neostriatum / cytology
  • Neostriatum / physiology
  • Neurons / enzymology*
  • Nitric Oxide Synthase / genetics*
  • Nitric Oxide Synthase / metabolism

Substances

  • Nitric Oxide Synthase