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首页> 外文期刊>The Journal of Comparative Neurology >Brain-derived neurotrophic factor promotes cochlear spiral ganglion cell survival and function in deafened, developing cats.
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Brain-derived neurotrophic factor promotes cochlear spiral ganglion cell survival and function in deafened, developing cats.

机译：脑源性神经营养因子可促进耳聋，发育中的猫的耳蜗螺旋神经节细胞存活和功能。

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Postnatal development and survival of spiral ganglion (SG) neurons depend on both neural activity and neurotrophic support. Our previous studies showed that electrical stimulation from a cochlear implant only partially prevents SG degeneration after early deafness. Thus, neurotrophic agents that might be combined with an implant to improve neural survival are of interest. Recent studies reporting that brain-derived neurotrophic factor (BDNF) promotes SG survival after deafness have been conducted in rodents and limited to relatively short durations. Our study examined longer duration BDNF treatment in deafened cats that may better model the slow progression of SG degeneration in human cochleae, and this is the first study of BDNF in the developing auditory system. Kittens were deafened neonatally, implanted at 4-5 weeks with intracochlear electrodes containing a drug-delivery cannula, and BDNF or artificial perilymph was infused for 10 weeks from a miniosmotic pump. In BDNF-treated cochleae, SG cells grew to normal size and were significantly larger than cells on the contralateral side. However, their morphology was not completely normal, and many neurons lacked or had thinned perikaryl myelin. Unbiased stereology was employed to estimate SG cell density, independent of cell size. BDNF was effective in promoting significantly improved survival of SG neurons in these developing animals. BDNF treatment also resulted in higher density and larger size of myelinated radial nerve fibers, sprouting of fibers into the scala tympani, and improvement of electrically evoked auditory brainstem response thresholds. BDNF may have potential therapeutic value in the developing auditory system, but many serious obstacles currently preclude clinical application.
机译：螺旋神经节（SG）神经元的出生后发育和生存取决于神经活动和神经营养支持。我们以前的研究表明，耳蜗植入物的电刺激只能部分预防早期耳聋后SG变性。因此，可以与植入物组合以改善神经存活的神经营养剂受到关注。最近的研究报告说，在啮齿动物中进行了耳聋后脑源性神经营养因子（BDNF）促进了SG的存活，并且限于相对较短的持续时间。我们的研究检查了耳聋猫的BDNF治疗时间更长，这可能更好地模拟了人类耳蜗SG退化的缓慢进展，这是BDNF在发育中的听觉系统中的首次研究。将新生的小猫耳聋，在4-5周时植入包含药物递送套管的耳蜗内电极，并从微型渗透泵中注入BDNF或人工淋巴液10周。在BDNF处理的耳蜗中，SG细胞生长到正常大小，并且明显大于对侧的细胞。然而，它们的形态并不完全正常，许多神经元缺乏或稀有过环芳基髓磷脂。独立于细胞大小，采用无偏立体学估计SG细胞密度。 BDNF可有效促进这些发育中动物的SG神经元存活率显着提高。 BDNF治疗还导致髓鞘状radial神经纤维的密度更高，尺寸更大，纤维萌发入鼓膜鼓室，以及电诱发听觉脑干反应阈值的提高。 BDNF在发展中的听觉系统中可能具有潜在的治疗价值，但是目前许多严重的障碍阻碍了临床应用。

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