Background: Tinnitus is a common disorder that causes significant morbidity; however, the neurophysiological mechanism is not yet fully understood. A relationship between tinnitus and limbic system has been reported. As a significant component of the limbic system, the hippocampus plays an important role in various pathological processes, such as emotional disturbance, decreased learning ability, and deterioration of memory. This study was aimed to explore the role of the hippocampus in the generation of tinnitus by electrophysiological technology.
Methods: A tinnitus model was established in rats through intraperitoneal injection of salicylate (SA). Subsequently, the spontaneous firing rate (SFR) of neurons in the hippocampal CA1 area was recorded with in vivo multichannel recording technology to assess changes in excitability induced by SA. To investigate the effect of excitability changes of hippocampus on the auditory pathway, the hippocampus was electrically stimulated and neural excitability in the auditory cortex (AC) was monitored.
Results: Totally 65 neurons in the hippocampal CA1 area were recorded, 45 from the SA group (n = 5), and 20 from the saline group (n = 5). Two hours after treatment, mean SFR of neurons in the hippocampal CA1 area had significantly increased from 3.06 ± 0.36 Hz to 9.18 ± 1.30 Hz in the SA group (t = -4.521, P < 0.05), while no significant difference was observed in the saline group (2.66 ± 0.36 Hz vs. 2.16 ± 0.36 Hz, t = 0.902, P > 0.05). In the AC, 79.3% (157/198) of recorded neurons showed responses to electrical stimulation of the hippocampal CA1 area. Presumed pyramidal neurons were excited, while intermediate neurons were inhibited after electrical stimulation of the hippocampus.
Conclusions: The study shows that the hippocampus is excited in SA-induced tinnitus, and stimulation of hippocampus could modulate neuronal excitability of the AC. The hippocampus is involved in tinnitus and may also have a regulatory effect on the neural center.
大鼠耳鸣模型中海马CA1区神经元兴奋性对听觉传导通路的影响摘要背景：耳鸣是听觉系统疾病的常见症状。耳鸣的病因复杂，其发生的神经生理学机制尚不明确。边缘系统参与学习、记忆和情绪反应，既往研究发现，边缘系统与耳鸣发生有关。海马是边缘系统的重要组成部分，在情绪障碍、学习和记忆能力减退等许多病理过程中起到关键作用。本研究旨在为海马参与耳鸣发生提供电生理实验证据。 方法：本研究通过腹腔注射水杨酸盐构建耳鸣模型，并利用在体多通道记录技术记录海马CA1区神经元兴奋性变化情况。通过电刺激海马CA1区记录听皮层神经元兴奋性变化，进一步研究海马CA1区神经元兴奋性改变对听觉传导通路的影响。 结果：本研究共记录到65个海马CA1区神经元，其中水杨酸盐组（n = 5）记录到45个，生理盐水组（n = 5）记录到20个。腹腔注射后2 h，水杨酸盐组海马CA1区神经元平均自发放电率从3.06 ± 0.36 Hz升高至9.08 ± 1.30 Hz（t = −4.521，P < 0.05），而生理盐水组未见显著变化（2.66 ± 0.36 Hz vs. 2.16 ± 0.36 Hz，t = 0.902，P > 0.05）。79.3 %（157/198）的听皮层神经元对海马CA1区电刺激有反应。电刺激海马CA1 区后，听皮层锥体神经元兴奋性增加，中间神经元兴奋性降低。 结论：水杨酸盐可引起海马区神经元兴奋性增加，海马CA1区电刺激可调节听皮层神经元的兴奋性。海马可能参与耳鸣发生，并参与耳鸣信号的调控。.
Keywords: Auditory Cortex; Electrical Stimulation; Hippocampus; Neuronal Excitability; Tinnitus.