Plasticity of synaptic endings in the cochlear nucleus following noise-induced hearing loss is facilitated in the adult FGF2 overexpressor mouse
Plasticity of synaptic endings in the cochlear nucleus following noise-induced hearing loss is facilitated in the adult FGF2 overexpressor mouse
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DOI：
10.1111/j.1460-9568.2007.05695.x
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发表时间：
2007-08-01
影响因子：
3.4
通讯作者：
Morest, D. Kent
中科院分区：
文献类型：
--
作者：
D'Sa, Chrystal;Gross, Julia;Morest, D. Kent
在成年哺乳动物中，单次暴露于大噪音可损伤耳蜗毛细胞并引发随后的耳蜗核轴突末梢变性发作。可能的机制是营养支持丧失和/或兴奋性毒性。成纤维细胞生长因子2 （FGF2）对发育很重要，可能参与其中的任何一种机制。为了验证这一假设，我们在噪声暴露后的1,2,4和8周，对FGF2过表达小鼠进行噪声暴露，并通过免疫标记SV2（一种突触囊泡蛋白）观察对突触末梢的影响。两个主要部位可见SV2染色；外周，代表轴-体细胞终端，和神经节，代表轴-树突终端。野生型（WT）失去了周围和神经细胞簇，中间有一段时间的周围恢复适度。相比之下，在过表达者中，在间隔时间增加后，周围细胞簇保持不变。神经细胞簇经历了一段时间的初始下降，随后是短暂的恢复和最终的下降。SV2免疫染色的变化与突触上谷氨酸囊泡和GABA转运蛋白的变化相关，在过表达者中，与FGF2和FGF受体1的染色变化相关。这些分子可能参与噪声损伤后突触的重组；它们可以保护和/或帮助过度刺激后的突触恢复。
In adult mammals a single exposure to loud noise can damage cochlear hair cells and initiate subsequent episodes of degeneration of axonal endings in the cochlear nucleus (CN). Possible mechanisms are loss of trophic support and/or excitotoxicity. Fibroblast growth factor 2 (FGF2), important for development, might be involved in either mechanism. To test this hypothesis, we noise-exposed FGF2 overexpressor mice and observed the effects on synaptic endings by immunolabelling for SV2, a synaptic vesicle protein, at 1, 2, 4, and 8 weeks after noise exposure. SV2 staining was observed in two major locations; perisomatic, representing axo-somatic terminals, and neuropil, representing axo-dendritic terminals. The wildtype (WT) lost both perisomatic and neuropil clusters with an intervening period of modest recovery for the perisomatic. In contrast, in the overexpressor, the perisomatic clusters remained unchanged after intervening periods of increase. The neuropil clusters underwent a period of initial decline, followed by a transient recovery and ultimate decline. Changes in SV2 immunostaining correlated with changes in vesicular glutamate and GABA transporters at synapses and, in the overexpressor, with staining changes for FGF2 and FGF receptor 1. These molecules may contribute to the synaptic reorganization after noise damage; they may protect and/or aid recovery of synapses after overstimulation.