Akbarnejad Zeinab, Bagherian Kasra, Noorbakhsh Seyed Ali, Jouzdani Ali Fathi, Mahmoudian Saeid, Mirsalehi Marjan, Jafarian Maryam, Mohammadi Ronak, Asghari Alimohamad, Asadpour Abdoreza
ENT and Head and Neck Research Center and Department, The Five Senses Health Institute, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Science Beam Institute, Istanbul, Turkey.
Brain Behav. 2025 Sep;15(9):e70795. doi: 10.1002/brb3.70795.
Tinnitus, a self-reported perceptual disorder, is currently believed to arise from maladaptive plasticity due to reduced sensory input. While deep brain stimulation (DBS) has shown promise in alleviating tinnitus-related behaviors, its effects on neuronal activity remain unclear. This study aimed to evaluate the spontaneous firing rates (SFRs) of the primary auditory cortex (A1) before and after DBS of the external cortex of the inferior colliculus (ECIC) in a rat model of tinnitus.
Tinnitus was induced in rats through sodium salicylate injections for 14 consecutive days, while the control group received normal saline injections over the same period. We conducted tinnitus and hearing assessments using the gap pre-pulse inhibition of the acoustic startle (GPIAS) and pre-pulse inhibition (PPI) tests. From day 14, both groups underwent DBS of the ECIC and single unit recordings from the A1.
Before ECIC stimulation, A1 neurons in rats with potential tinnitus exhibited significantly higher spontaneous activity compared to controls. Following ECIC stimulation, the SFRs in the group displaying abnormal GPIAS responses significantly decreased, and the difference between the tinnitus and control groups was no longer significant. Additionally, inter-spike interval (ISI) analysis revealed a higher frequency of short ISIs (<5 ms) in rats with potential tinnitus, which decreased after DBS, aligning with values observed in the control group.
ECIC stimulation effectively modulates A1 hyperactivity, highlighting its role in tinnitus pathophysiology. These findings warrant further research into ECIC's role in tinnitus regulation, which could inform future therapeutic interventions and enhance mathematical models of tinnitus mechanisms.
耳鸣是一种自我报告的感知障碍，目前认为是由于感觉输入减少导致的适应性不良可塑性引起的。虽然深部脑刺激（DBS）在减轻耳鸣相关行为方面显示出前景，但其对神经元活动的影响仍不清楚。本研究旨在评估在耳鸣大鼠模型中，刺激下丘外侧皮质（ECIC）前后初级听觉皮层（A1）的自发放电率（SFRs）。
通过连续14天注射水杨酸钠诱导大鼠耳鸣，而对照组在同一时期注射生理盐水。我们使用听觉惊吓的间隙前脉冲抑制（GPIAS）和前脉冲抑制（PPI）测试进行耳鸣和听力评估。从第14天开始，两组均接受ECIC的DBS并从A1进行单单位记录。
在ECIC刺激前，有潜在耳鸣的大鼠的A1神经元表现出比对照组显著更高的自发活动。在ECIC刺激后，显示异常GPIAS反应的组中的SFRs显著降低，耳鸣组和对照组之间的差异不再显著。此外，峰间期（ISI）分析显示，有潜在耳鸣的大鼠中短ISI（<5毫秒）的频率更高，DBS后降低，与对照组观察到的值一致。
ECIC刺激有效地调节A1的过度活动，突出了其在耳鸣病理生理学中的作用。这些发现值得进一步研究ECIC在耳鸣调节中的作用，这可能为未来的治疗干预提供信息并增强耳鸣机制的数学模型。
