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Nitric oxide increases gain in the ventral cochlear nucleus of guinea pigs with tinnitus.
European Journal of Neroscience ( IF 3.4 ) Pub Date : 2020-07-19 , DOI: 10.1111/ejn.14913 Adam Hockley 1, 2, 3 , Joel I Berger 1, 4 , Alan R Palmer 1, 5 , Mark N Wallace 1, 5
European Journal of Neroscience ( IF 3.4 ) Pub Date : 2020-07-19 , DOI: 10.1111/ejn.14913 Adam Hockley 1, 2, 3 , Joel I Berger 1, 4 , Alan R Palmer 1, 5 , Mark N Wallace 1, 5
Affiliation
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.
中文翻译:
一氧化氮增加耳鸣豚鼠腹侧耳蜗核的增益。
以前的工作导致了这样一个假设,即在产生噪音引起的耳鸣期间,腹侧耳蜗核 (VCN) 中较高水平的一氧化氮 (NO) 会增加应用于耳蜗输入减少的增益。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 只耳鸣的证据,然后比较了离子电渗应用的 NO 供体或生成抑制剂对 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是相同的,而在非耳鸣组则有所下降。相比之下,耳鸣组的平均自发率相对于对照组有所增加,而非耳鸣组的平均自发率保持不变。在耳鸣组(56%)和非耳鸣组(71%),与对照组(24%)相比,更大比例的单位对外源性 NO 有反应。在耳鸣组中,内源性 NO 促进了 37% (7/19) 神经元的驱动放电率,并且似乎通过涉及 N-甲基-D-天冬氨酸 (NMDA) 的机制使平均驱动率恢复到控制水平受体。相比之下,在非耳鸣组中,内源性 NO 仅促进 5% (1/22) 的神经元的驱动放电率,而在对照组中没有促进驱动率。内源性 NO 对自发活动的影响尚不清楚。这些结果表明,NO 参与增加了应用于驱动活动的增益,但其他因素也参与了自发活动的增加。
更新日期:2020-07-19
中文翻译:
一氧化氮增加耳鸣豚鼠腹侧耳蜗核的增益。
以前的工作导致了这样一个假设,即在产生噪音引起的耳鸣期间,腹侧耳蜗核 (VCN) 中较高水平的一氧化氮 (NO) 会增加应用于耳蜗输入减少的增益。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 只耳鸣的证据,然后比较了离子电渗应用的 NO 供体或生成抑制剂对 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是相同的,而在非耳鸣组则有所下降。相比之下,耳鸣组的平均自发率相对于对照组有所增加,而非耳鸣组的平均自发率保持不变。在耳鸣组(56%)和非耳鸣组(71%),与对照组(24%)相比,更大比例的单位对外源性 NO 有反应。在耳鸣组中,内源性 NO 促进了 37% (7/19) 神经元的驱动放电率,并且似乎通过涉及 N-甲基-D-天冬氨酸 (NMDA) 的机制使平均驱动率恢复到控制水平受体。相比之下,在非耳鸣组中,内源性 NO 仅促进 5% (1/22) 的神经元的驱动放电率,而在对照组中没有促进驱动率。内源性 NO 对自发活动的影响尚不清楚。这些结果表明,NO 参与增加了应用于驱动活动的增益,但其他因素也参与了自发活动的增加。