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首页> 外文期刊>The European Journal of Neuroscience >Exogenous nitric oxide causes potentiation of hippocampal synaptic transmission during low-frequency stimulation via the endogenous nitric oxide-cGMP pathway.
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Exogenous nitric oxide causes potentiation of hippocampal synaptic transmission during low-frequency stimulation via the endogenous nitric oxide-cGMP pathway.

机译：外源性一氧化氮在低频刺激过程中通过内源性一氧化氮-cGMP途径引起海马突触传递的增强。

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摘要

Nitric oxide (NO) is a putative participant in synaptic plasticity and demonstrations that exogenous NO can elicit the same plastic changes have been taken to support such a role. The experiments, carried out on the CA1 region of rat hippocampal slices, were aimed at testing this interpretation. A major component of tetanus-induced long-term potentiation (LTP) was lost in response to L-nitroarginine, which inhibits NO synthase, and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), which inhibits NO-sensitive soluble guanylyl cyclase (sGC). At 0.2 Hz afferent fibre stimulation, exogenous NO produced, concentration-dependently, a synaptic depression that reverted on washout to a persistent potentiation that occluded tetanus-induced LTP. The NO concentrations necessary (estimated in the 100-nM range), however, were mostly supramaximal for stimulating hippocampal slice sGC activity. Nevertheless the potentiation, but not the preceding depression, was blocked by ODQ. L-nitroarginine and an NMDA antagonist were similarly effective, indicating mediation by the endogenous NMDA receptor-NO synthase-sGC pathway. At a concentration normally too low to affect synaptic transmission but sufficient to stimulate sGC (estimated to be 50 nM), exogenous NO reversed the effect of L-nitroarginine and caused a potentiation which was blocked by ODQ. At a concentration inducing the depression/potentiation sequence, NO partially inhibited hippocampal slice oxygen consumption. It is concluded that, at physiological levels, exogenous NO can directly elicit a potentiation of synaptic transmission through sGC, provided that the synapses are suitably primed. At higher concentrations, NO inhibits mitochondrial respiration, which can result in an enduring synaptic potentiation due to secondary activation of the endogenous NO-cGMP pathway.
机译：一氧化氮（NO）是突触可塑性的假定参与者，并且已证明外源NO可以引起相同的塑性变化以支持这种作用。在大鼠海马切片的CA1区进行的实验旨在测试这种解释。破伤风诱导的长期增强作用（LTP）的主要成分因抑制NO合酶的L-硝基精氨酸和1H- [1,2,4] oxadiazolo [4,3-a] quinoxalin-1-而丢失一种（ODQ），其抑制NO敏感的可溶性鸟苷酸环化酶（sGC）。在0.2 Hz的传入纤维刺激下，外源性NO产生浓度依赖性的突触抑制，该抑制在冲刷时恢复为持续的增强作用，从而使破伤风诱导的LTP闭塞。但是，必需的NO浓度（估计在100-nM范围内）对于刺激海马切片sGC活性而言大多是最大的。但是，ODQ阻止了这种增强作用，但先前的抑制作用却没有。 L-硝基精氨酸和NMDA拮抗剂具有相似的效果，表明可通过内源性NMDA受体-NO合酶-sGC途径介导。在通常太低而不能影响突触传递但足以刺激sGC的浓度（估计为50 nM）下，外源NO逆转了L-硝基精氨酸的作用，并引起了被ODQ阻断的增强作用。在诱导降低/增强序列的浓度下，NO部分抑制海马片的耗氧量。结论是，在生理水平上，外源NO可以直接引发通过sGC的突触传递增强作用，前提是适当地引发突触。在较高浓度下，NO抑制线粒体呼吸，由于内源性NO-cGMP途径的二次激活，可导致持久的突触增强。

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