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Initial studies on the direct and modulatory effects of nitric oxide on an identified central Helix aspersa neuron.
Invertebrate Neuroscience Pub Date : 2014-11-08 , DOI: 10.1007/s10158-014-0175-3
Nicholas J D Wright 1 , Lynda J Sides , Kerry Walling
Affiliation  

The generation of the novel messenger molecule nitric oxide (NO) has been demonstrated in many tissues across phyla including nervous systems. It is produced on demand by the enzyme nitric oxide synthase often stimulated by intracellular calcium and typically affecting guanylate cyclase thought to be its principal target in an auto and/or paracrine fashion. This results in the generation of the secondary messenger cyclic guanosine monophosphate (cGMP). Nitric oxide synthase has been demonstrated in various mollusk brains and manipulation of NO levels has been shown to affect behavior in mollusks. Apart from modulation of the effect of the peptide GSPYFVamide, there appears little published on direct or modulatory effects of NO on Helix aspersa central neurons. We present here initial results to show that NO can be generated in the region around F1 in the right parietal ganglion and that NO and cGMP directly hyperpolarize this neuron. For example, application of the NO-donor S-nitroso-N-acetyl-d,l-penicillamine (SNAP; 200 µM) can cause a mean hyperpolarization of 41.7 mV, while 2 mM 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP) produced a mean hyperpolarization of 33.4 mV. Additionally, pre-exposure to NO-donors or cGMP appears to significantly reduce or even eliminates the normal hyperpolarizing K+-mediated response to dopamine (DA) by this neuron; 200 µM SNAP abolishes a standard response to 0.5 µM DA while 1 mM 8-bromo-cGMP reduces it 62 %.

中文翻译:

一氧化氮对已确定的中枢螺旋曲霉神经元的直接和调节作用的初步研究。

新型信使分子一氧化氮(NO)的产生已在整个门的许多组织(包括神经系统)中得到证实。它是由经常被细胞内钙刺激并通常影响鸟苷酸环化酶的一氧化氮合酶按需生产的,而鸟苷酸环化酶被认为是自体和/或旁分泌方式的主要靶标。这导致产生第二信使环鸟苷单磷酸酯(cGMP)。一氧化氮合酶已在各种软体动物的大脑中得到证实,并且NO水平的变化已证明会影响软体动物的行为。除了肽GSPYFVamide的效果调制,出现小发表了对NO的直接或调节作用花园蜗牛中枢神经元。我们在这里提供的初步结果表明,可以在右顶神经节的F1周围区域生成NO,并且NO和cGMP直接使该神经元超极化。例如,使用NO供体S-硝基-N-乙酰基-d1-青霉胺(SNAP; 200 µM)可以导致平均超极化41.7 mV,而2 mM 8-溴环鸟苷单磷酸(8- bromo-cGMP)产生33.4 mV的平均超极化。此外,预先暴露于NO供体或cGMP似乎会显着减少甚至消除正常的超极化K +该神经元介导的对多巴胺(DA)的反应;200 µM SNAP消除了对0.5 µM DA的标准响应,而1 mM 8-bromo-cGMP降低了62%。
更新日期:2014-11-08
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