Zorumski C F, Izumi Y
Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USA.
Prog Brain Res. 1998;118:173-82. doi: 10.1016/s0079-6123(08)63207-0.
In the CA1 hippocampal region, the induction of long-term potentiation (LTP) requires activation of N-methyl-D-aspartate receptors (NMDARs). However, untimely NMDAR activation either immediately prior to or following tetanic stimulation inhibits LTP generation. This NMDAR-mediated LTP inhibition is overcome by inhibitors of nitric oxide synthase (NOS) and hemoglobin, suggesting the involvement of NO. Additionally, NO inhibitors can promote the ability of weak tetanic stimuli to produce LTP under basal conditions in hippocampal slices. Recent experiments indicate that untimely NMDAR activation contributes to the failure of LTP induction during periods of low glucose exposure and hypoxia. Following hypoxia there is also a delayed form of LTP inhibition that is reversed by NMDAR antagonists and NO inhibitors. These results suggest that there are physiological and pathological conditions during which NMDAR activation and NO release modulate the induction of synaptic plasticity.
在海马体CA1区，长时程增强（LTP）的诱导需要N-甲基-D-天冬氨酸受体（NMDARs）的激活。然而，在强直刺激之前或之后过早激活NMDAR会抑制LTP的产生。一氧化氮合酶（NOS）抑制剂和血红蛋白可克服这种由NMDAR介导的LTP抑制，提示一氧化氮（NO）参与其中。此外，NO抑制剂可增强弱强直刺激在基础条件下诱导海马切片产生LTP的能力。最近的实验表明，过早激活NMDAR会导致在低葡萄糖暴露和缺氧期间LTP诱导失败。缺氧后还存在一种延迟形式的LTP抑制，可被NMDAR拮抗剂和NO抑制剂逆转。这些结果表明，在某些生理和病理条件下，NMDAR激活和NO释放会调节突触可塑性的诱导。
