海人酸对鸡耳声发射和耳蜗电位的兴奋毒性作用。
Excitotoxic effect of kainic acid on chicken otoacoustic emissions and cochlear potentials.
作者信息
Sun H, Salvi R J, Ding D L, Hashino D E, Shero M, Zheng X Y
机构信息
Center for Hearing and Deafness, SUNY State University at Buffalo, New York 14214, USA.
出版信息
J Acoust Soc Am. 2000 Apr;107(4):2136-42. doi: 10.1121/1.428495.
Kainic acid (KA) is a potent glutamate analog that can temporarily or permanently damage glutamatergic neurons. The purpose of the present study was to determine the short- and long-term effects of KA on chicken otoacoustic emissions and cochlear potentials. A chronic electrode was used to record the compound action potential (CAP), cochlear microphonic (CM), and the slow, positive neural potential (SPNP), a predominantly dc response. The CM, CAP, SPNP, and distortion product otoacoustic emissions (DPOAEs) were recorded before and after infusing 10 microl of a low dose (KA-L, 0.3 mM) or high dose (KA-H, 5 mM) of KA into scala tympani. KA caused a rapid and large reduction in CAP and SPNP amplitude in both the KA-H and KA-L groups; however, the CM and DPOAEs were largely unchanged. The amplitude of the CAP and SPNP in the KA-L group began to recover around 1 week post-KA, but was approximately 50% below normal at 4 weeks post-KA. In contrast, the CAP and SPNP showed no signs of recovery in the KA-H group. The results suggest that KA has no effect on the CM and DPOAEs generated by the hair cells, but selectively damages the CAP generated by the cochlear ganglion neurons. The reduction in the avian SPNP suggests that the response originates in the cochlear afferent neurons, unlike the summating potential (SP) in mammals that is generated in hair cells.
kainic 酸（KA）是一种强效谷氨酸类似物，可暂时或永久性损伤谷氨酸能神经元。本研究的目的是确定 KA 对鸡耳声发射和耳蜗电位的短期和长期影响。使用慢性电极记录复合动作电位（CAP）、耳蜗微音电位（CM）和缓慢的正向神经电位（SPNP），后者主要是直流反应。在向鼓阶注入 10 微升低剂量（KA-L，0.3 mM）或高剂量（KA-H，5 mM）的 KA 之前和之后，记录 CM、CAP、SPNP 和畸变产物耳声发射（DPOAE）。KA 在 KA-H 组和 KA-L 组中均导致 CAP 和 SPNP 幅度迅速大幅降低；然而，CM 和 DPOAE 基本未变。KA-L 组中 CAP 和 SPNP 的幅度在 KA 后约 1 周开始恢复，但在 KA 后 4 周比正常水平低约 50%。相比之下，KA-H 组中 CAP 和 SPNP 没有恢复迹象。结果表明，KA 对毛细胞产生的 CM 和 DPOAE 没有影响，但选择性地损害耳蜗神经节神经元产生的 CAP。禽类 SPNP 的降低表明该反应起源于耳蜗传入神经元，这与哺乳动物中在毛细胞中产生的总和电位（SP）不同。
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