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本研究通过制作急性水杨酸(salicylate acid,SA)大鼠耳鸣模型,观察电刺激初级听皮层(primary auditory cortex,AI)对下丘外侧核(external nucleus of inferior colliculus,ICx)放电活动的影响,探讨听觉的下行调控对耳鸣相关放电活动的作用。采用立体定位技术及细胞外记录方法,记录电刺激左侧AI后同侧ICx放电活动变化,用平均自发放电率和放电间隔直方图为观察指标。电刺激AI前、后持续记录急性SA模型大鼠同一ICx神经元自发放电。结果显示,电刺激AI对较高放电率的ICx神经元起抑制作用,对较低放电率的ICx神经元起易化作用。从ICx神经元平均自发放电率和短间隔放电比例来分析,电刺激AI后的4h观察时间内,对正常组与急性SA模型组大鼠ICx神经元放电均起抑制作用,而对急性SA模型组大鼠的抑制作用比对正常大鼠的抑制作用持久。上述结果提示,电刺激AI通过下行通路调控可在一段时间内抑制SA引起的与耳鸣相关的ICx放电活动。
In this study, the effects of electrical stimulation of primary auditory cortex (AI) on the discharge activity of the external nucleus of inferior colliculus (ICx) were observed by making a tinnitus model of acute salicylate acid (SA) , To explore the role of downward hearing-related regulation of tinnitus-related discharge activity. Stereotactic and extracellular recording methods were used to record the changes of ipsilateral ICx discharge activity after electrical stimulation of the left AI. The average spontaneous firing rate and discharge interval histogram were used as the observation indexes. Before and after electrical stimulation of AI, spontaneous discharges of the same ICx neurons in the acute SA model rats were recorded continuously. The results showed that electrical stimulation of AI inhibited ICx neurons with higher discharge rate and facilitated ICx neurons with lower discharge rate. From the average spontaneous firing rates of ICx neurons and the proportion of short-interval discharges, IC4 neurons in both normal and acute SA models were inhibited in the 4h observation period after electrical stimulation of AI, while the acute SA model The inhibitory effect of the group of rats longer than the normal rats. These results suggest that electrical stimulation of AI via downstream pathway regulation may inhibit SA-induced tinnitus-related ICx discharge activity over a period of time.