Nitric Oxide Synthase Inhibition In Vivo: Lack of Effect on Hippocampal SynapticEnhancement or Spatial Memory~199

摘要

Experiments performed on the in vitro hippocampal slice or cell culturepreparations suggest that nitric oxide (NO) may translate induction events into expression of long-term enhancement (LTP/LTE) of synapses in hippocampal subfield CAI (Bohme et al., 1991) O'Dell et al., 1991; Schuman and Madison, 1991; (Haley et al., 1992). NO synthesis is presumably triggered postsynaptically through the activation of NMDA receptors, which leads to calcium influx, calmodulin binding, and nitric oxide synthase (NOS) activation (Garthwaite et al., 1988, 1989; Fujimori and Pan-Hou, 1991). The release of NO from postsynaptic neurons appears to increase transmitter release from terminals near the site of NO release (Schuman and Madison, 1991); however, such a presynaptic mechanism for the expression of LTE has been the subject of controversy (Bekkers and Stevens, 1990: Malinow and Tsien, 1990; Foster and McNaughton, 1991; Manabe et al., 1992). In the hippocampus, the highest levels of NOS are present in the fascia dentata (FD), although the CAl pyramidal cells stain for the NADPH-diaphorase isoform, which has been found to have a neuronal distribution coincident with NOS (Bredt and Snyder, 1990; Bredt et al., 1991: Dawson et al., 1991).