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首页> 美国卫生研究院文献>JARO: Journal of the Association for Research in Otolaryngology >Enhanced Survival of Spiral Ganglion Cells After Cessation of Treatment with Brain-Derived Neurotrophic Factor in Deafened Guinea Pigs
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Enhanced Survival of Spiral Ganglion Cells After Cessation of Treatment with Brain-Derived Neurotrophic Factor in Deafened Guinea Pigs

机译：失聪的豚鼠停止脑源性神经营养因子治疗后螺旋神经节细胞存活率提高

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Exogenous delivery of neurotrophic factors into the cochlea of deafened animals rescues spiral ganglion cells (SGCs) from degeneration. To be clinically relevant for human cochlear implant candidates, the protective effect of neurotrophins should persist after cessation of treatment and the treated SGCs should remain functional. In this study, the survival and functionality of SGCs were investigated after temporary treatment with brain-derived neurotrophic factor (BDNF). Guinea pigs in the experimental group were deafened, and 2 weeks later, the right cochleae were implanted with an electrode array and drug delivery cannula. BDNF was administered to the implanted cochleae during a 4-week period via a mini-osmotic pump. After completion of the treatment, the osmotic pumps were removed. Two weeks later, the animals were killed and the survival of SGCs was analyzed. To monitor the functionality of the auditory nerve, electrically evoked auditory brainstem responses (eABRs) were recorded in awake animals throughout the experiment. BDNF treatment resulted in enhanced survival of SGCs 2 weeks after cessation of the treatment and prevented the decreases in size and circularity that are seen in the untreated contralateral cochleae. The amplitude of the suprathreshold eABR response in BDNF-treated animals was significantly larger than in deafened control animals and comparable to that in normal-hearing control animals. The amplitude in the BDNF-treated group did not decrease significantly after cessation of treatment. The eABR latency in BDNF-treated animals was longer than normal and comparable to that in deafened control animals. These morphological and functional findings demonstrate that neurotrophic intervention had a lasting effect, which is promising for future clinical application of neurotrophic factors in implanted human cochleae.
机译：将神经营养因子外源传递到失聪动物的耳蜗中，可以拯救螺旋神经节细胞（SGC）的变性。为了与候选人类人工耳蜗在临床上相关，神经营养蛋白的保护作用应在停止治疗后继续存在，并且所治疗的SGC应保持功能正常。在这项研究中，对临时性脑源性神经营养因子（BDNF）治疗后的SGC的存活和功能进行了研究。实验组的豚鼠耳聋，2周后，右耳蜗植入电极阵列和药物输送套管。 BDNF通过微型渗透泵在4周内施用于植入的耳蜗。处理完成后，将渗透泵卸下。两周后，处死动物并分析了SGC的存活。为了监测听觉神经的功能，在整个实验过程中，在清醒的动物中记录了电诱发的听觉脑干反应（eABR）。 BDNF治疗可在停止治疗后2周提高SGC的存活率，并防止未治疗的对侧耳蜗看到的大小和圆形度降低。在BDNF治疗的动物中，阈上eABR应答的幅度明显大于失聪的对照动物，并且与正常听力的对照动物相当。停止治疗后，BDNF治疗组的振幅没有明显降低。在BDNF处理的动物中，eABR潜伏期比正常人更长，并且与失聪的对照动物相比。这些形态和功能上的发现表明，神经营养干预具有持久的作用，这对于神经营养因子在植入人耳蜗的未来临床应用是有前途的。

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