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前扣带皮层参与水杨酸钠诱导的耳鸣。

Participation of the Anterior Cingulate Cortex in Sodium Salicylate-induced Tinnitus.

机构信息

Department of Otolaryngology Head and Neck Surgery, Peking University Third Hospital.

Beijing National Laboratory for Molecular Sciences, Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, The Chinese Academy of Sciences, Beijing, China.

出版信息

Otol Neurotol. 2021 Sep 1;42(8):e1134-e1142. doi: 10.1097/MAO.0000000000003183.

DOI:10.1097/MAO.0000000000003183
PMID:33859133
Abstract

HYPOTHESIS

The anterior cingulate cortex (ACC) participates in sodium salicylate (SS)-induced tinnitus through alteration of the disordered neural activity and modulates the neuronal changes in the auditory cortex (AC).

BACKGROUND

Although the mechanism underlying tinnitus remains unclear, the crucial roles of the auditory center and limbic system in this process have been elucidated. Recent reports suggest that dysfunction of the ACC, an important component of the limbic system that regulates and controls the conduction of multiple sensations, is involved in tinnitus. Although altered functional connectivity between the ACC and the auditory system has been observed in humans with tinnitus, the underlying neuronal mechanism remains unexplored.

METHODS

SS (350 mg/kg, 10%, i.p.) was used to yield tinnitus model in rats, followed by comparison of the alteration in the spontaneous firing rate (SFR), local field potential (LFP), and extracellular glutamic acid in the ACC. The responses of neurons in the AC to electrical stimulation from the ACC were also observed.

RESULTS

We determined significant increases in the neuronal SFR and extracellular glutamate level in the ACC after SS injection (p < 0.05). These effects were accompanied by decreased alpha band activity and increased beta and gamma band activity (p < 0.05). In the majority of AC neurons, the SFR decreased in response to ACC stimulation (p < 0.05).

CONCLUSIONS

Our results demonstrated that disordered neural activity in the ACC contributes to SS-induced tinnitus and that ACC activation can modulate AC activity.

摘要

假设

前扣带皮层(ACC)通过改变紊乱的神经活动参与到水杨酸钠(SS)诱导的耳鸣中,并调节听觉皮层(AC)中的神经元变化。

背景

尽管耳鸣的机制仍不清楚,但听觉中枢和边缘系统在这一过程中的关键作用已经阐明。最近的报告表明,调节和控制多种感觉传导的边缘系统的重要组成部分——ACC 的功能障碍与耳鸣有关。尽管在耳鸣患者中观察到 ACC 与听觉系统之间的功能连接改变,但潜在的神经元机制仍未得到探索。

方法

使用 SS(350mg/kg,10%,腹腔注射)在大鼠中产生耳鸣模型,然后比较 ACC 中自发性放电率(SFR)、局部场电位(LFP)和细胞外谷氨酸的变化。还观察了 ACC 对 AC 神经元电刺激的反应。

结果

我们确定 SS 注射后 ACC 中的神经元 SFR 和细胞外谷氨酸水平显著增加(p<0.05)。这些效应伴随着 alpha 波段活动的减少和 beta 和 gamma 波段活动的增加(p<0.05)。在大多数 AC 神经元中,ACC 刺激导致 SFR 降低(p<0.05)。

结论

我们的结果表明,ACC 中紊乱的神经活动导致 SS 诱导的耳鸣,并且 ACC 的激活可以调节 AC 的活动。

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引用本文的文献

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Decoding tinnitus progression: neurochemical shifts in the anterior cingulate cortex revealed by magnetic resonance spectroscopy.解码耳鸣进展:磁共振波谱揭示前扣带回皮质的神经化学变化
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Functional Connectivity Alterations and Molecular Characterization of the Anterior Cingulate Cortex in Tinnitus Pathology without Hearing Loss.无听力损失耳鸣患者前扣带回皮层的功能连接改变及分子特征。
Adv Sci (Weinh). 2024 Jan;11(3):e2304709. doi: 10.1002/advs.202304709. Epub 2023 Nov 27.