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首页> 外文期刊>The European Journal of Neuroscience >Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus
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Nitric oxide regulates the firing rate of neuronal subtypes in the guinea pig ventral cochlear nucleus

机译：一氧化氮调节豚鼠腹部耳蜗核中神经元亚型的烧制率

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The gaseous free radical, nitric oxide (NO) acts as a ubiquitous neuromodulator, contributing to synaptic plasticity in a complex way that can involve either long term potentiation or depression. It is produced by neuronal nitric oxide synthase (nNOS) which is presynaptically expressed and also located postsynaptically in the membrane and cytoplasm of a subpopulation of each major neuronal type in the ventral cochlear nucleus (VCN). We have used iontophoresis in vivo to study the effect of the NOS inhibitor L-NAME (L-NG-Nitroarginine methyl ester) and the NO donors SIN-1 (3-Morpholinosydnonimine hydrochloride) and SNOG (S-Nitrosoglutathione) on VCN units under urethane anaesthesia. Collectively, both donors produced increases and decreases in driven and spontaneous firing rates of some neurones. Inhibition of endogenous NO production with L-NAME evoked a consistent increase in driven firing rates in 18% of units without much effect on spontaneous rate. This reduction of gain produced by endogenous NO was mirrored when studying the effect of L-NAME on NMDA(N-Methyl-D-aspartic acid)-evoked excitation, with 30% of units showing enhanced NMDA-evoked excitation during L-NAME application (reduced NO levels). Approximately 25% of neurones contain nNOS and the NO produced can modulate the firing rate of the main principal cells: medium stellates (choppers), large stellates (onset responses) and bushy cells (primary-like responses). The main endogenous role of NO seems to be to partly suppress driven firing rates associated with NMDA channel activity but there is scope for it to increase neural gain if there were a pathological increase in its production following hearing loss.
机译：气体自由基，一氧化氮（NO）用作普遍存在的神经调节剂，以涉及长期增强或抑郁症的复杂方式有助于突触可塑性。它由神经元一氧化氮合酶（NNO）产生，其突出地表达并在腹侧耳蜗核（VCN）中的每个主要神经元类型的亚群的膜和细胞质中突触地定位。我们在体内使用离子电渗疗法以研究NoS抑制剂L-名称（L-Ng-Nitroarginine甲酯）和NO供体Sin-1（3-硫胺糖氨基胺盐酸盐）和SNOG（S-NITROSOGLUTATHIONE）的效果在VCN单元上氨基甲酸酯麻醉。统称，两种供体产生的一些神经元的驱动和自发射击率产生增加和减少。抑制内源性没有L-Name的生产诱发18％的单位的驱动烧制率一致增加，而不是对自发率有很大影响。当研究L-NAME对NMDA（N-甲基-D-天冬氨酸）释放的效果时，通过内源性NO产生的增益减少，其中30％的单位显示在L名申请期间显示增强的NMDA诱发激发（减少没有级别）。大约25％的神经元含有NNO，NNOS可以调节主要主体细胞的烧制率：培养基星状型（切孔），大星状响应（发病响应）和浓密细胞（初级响应）。非内源性的作用似乎是部分抑制与NMDA信道活动相关的驱动射击率，但如果在听力损失后的生产过程中存在病理增加，则会增加神经增益的范围。

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