Malen P L, Chapman P F
Graduate Program in Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA.
J Neurosci. 1997 Apr 1;17(7):2645-51. doi: 10.1523/JNEUROSCI.17-07-02645.1997.
Reports that nitric oxide synthase (NOS) inhibition prevents the induction of long-term potentiation (LTP) have been controversial. Recent evidence suggests that NO may help to regulate the threshold for LTP induction. We have tested this hypothesis by examining the effects of stimulus frequency and train duration on synaptic plasticity in the presence of either NO donors or NOS inhibitors. Two different NO donors facilitated LTP induction by stimuli that normally produced only short-term potentiation, whereas NOS inhibitors blocked LTP to stimuli that normally produce small LTP. NO donors facilitated LTP induction even when NMDA receptors were blocked, indicating that NO need not act via NMDA receptors. NO donors and NOS inhibitors were without effect on long-term depression (LTD), suggesting that they act on a distinct potentiating mechanism. Thus, NO could contribute to the establishment of plasticity under physiologically relevant conditions by selectively increasing the probability of LTP induction.
一氧化氮合酶（NOS）抑制可阻止长时程增强（LTP）诱导的报道一直存在争议。最近的证据表明，NO可能有助于调节LTP诱导的阈值。我们通过检查在存在NO供体或NOS抑制剂的情况下刺激频率和训练持续时间对突触可塑性的影响来检验这一假设。两种不同的NO供体通过通常仅产生短期增强的刺激促进了LTP诱导，而NOS抑制剂则阻断了对通常产生小幅度LTP的刺激的LTP。即使NMDA受体被阻断，NO供体仍促进LTP诱导，表明NO无需通过NMDA受体起作用。NO供体和NOS抑制剂对长时程抑制（LTD）没有影响，表明它们作用于一种独特的增强机制。因此，NO可能通过选择性增加LTP诱导的概率，在生理相关条件下有助于可塑性的建立。
