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首页> 外文期刊>The European Journal of Neuroscience >Nitric oxide increases gain in the ventral cochlear nucleus of guinea pigs with tinnitus
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Nitric oxide increases gain in the ventral cochlear nucleus of guinea pigs with tinnitus

机译：一氧化氮增加豚鼠的腹腔耳蜗核的增益增加

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Previous work has led to the hypothesis that, during the production of noise-induced tinnitus, higher levels of nitric oxide (NO), in the ventral cochlear nucleus (VCN), increase the gain applied to a reduced input from the cochlea. To test this hypothesis, we noise-exposed 26 guinea pigs, identified evidence of tinnitus in 12 of them and then compared the effects of an iontophoretically applied NO donor or production inhibitor on VCN single unit activity. We confirmed that the mean driven firing rate for the tinnitus and control groups was the same while it had fallen in the non-tinnitus group. By contrast, the mean spontaneous rate had increased for the tinnitus group relative to the control group, while it remained the same for the non-tinnitus group. A greater proportion of units responded to exogenously applied NO in the tinnitus (56%) and non-tinnitus groups (71%) than a control population (24%). In the tinnitus group, endogenous NO facilitated the driven firing rate in 37% (7/19) of neurons and appeared to bring the mean driven rate back up to control levels by a mechanism involving N-methyl-D-aspartic acid (NMDA) receptors. By contrast, in the non-tinnitus group, endogenous NO only facilitated the driven firing rate in 5% (1/22) of neurons and there was no facilitation of driven rate in the control group. The effects of endogenous NO on spontaneous activity were unclear. These results suggest that NO is involved in increasing the gain applied to driven activity, but other factors are also involved in the increase in spontaneous activity.
机译：之前的研究已经提出了这样的假设，即在噪声诱发耳鸣的产生过程中，耳蜗腹侧核（VCN）中较高水平的一氧化氮（NO）会增加应用于耳蜗减少输入的增益。为了验证这一假设，我们对26只豚鼠进行了噪声暴露，确定了其中12只豚鼠的耳鸣证据，然后比较了离子导入法应用NO供体或产生抑制剂对VCN单单位活性的影响。我们证实耳鸣组和对照组的平均驱动放电率相同，而非耳鸣组的平均驱动放电率有所下降。相比之下，与对照组相比，耳鸣组的平均自发频率有所增加，而非耳鸣组的平均自发频率保持不变。在耳鸣组（56%）和非耳鸣组（71%）中，对外源性应用NO有反应的单位比例高于对照组（24%）。在耳鸣组，内源性NO促进了37%（7/19）神经元的驱动放电率，并似乎通过涉及N-甲基-D-天冬氨酸（NMDA）受体的机制将平均驱动放电率恢复到控制水平。相比之下，在非耳鸣组，内源性NO仅促进5%（1/22）神经元的驱动放电率，而在对照组中，内源性NO不促进驱动放电率。内源性NO对自发活动的影响尚不清楚。这些结果表明，NO参与增加驱动活动的增益，但其他因素也参与自发活动的增加。

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