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[神经营养因子GDNF家族及其受体在正常听力和耳聋大鼠的螺旋神经节细胞中均可检测到]

[Neurotrophic factors of the GDNF family and their receptors are detectable in spiral ganglion cells of normal hearing as well as of deafened rats].

作者信息

Wefstaedt P, Scheper V, Rieger H, Lenarz T, Stöver T

机构信息

Hals-Nasen-Ohrenklinik der Medizinischen Hochschule Hannover.

出版信息

Laryngorhinootologie. 2006 Nov;85(11):802-8. doi: 10.1055/s-2006-925287. Epub 2006 Apr 10.

Abstract

BACKGROUND

Recent studies have shown that neurotrophic factors like BDNF, NT-3 and GDNF induce protective effects on spiral ganglion cells after noise- or drug-induced hearing loss. According to these studies it is suggested that deafness leads to a lack of neurotrophic factor or relating receptor expression in spiral ganglion cells, that has to be compensated by local cochlear application of these factors.

METHODS

In the present study we examined the expression pattern of members of the GDNF family (GDNF, Neurturin, Artemin, Persephin) and their relating receptors (Ret, GFRalpha1 - 3) as well as BDNF and trkB on spiral ganglion cells of normal hearing and experimentally deafened rats (10 % neomycine). Indirect immunofluorescence was carried out to determine protein expression of these factors and their receptors 26 days following deafening.

RESULTS

Our results demonstrate neurotrophic factor and receptor expression on spiral ganglion cells of normal hearing as well as experimentally deafened animals.

CONCLUSIONS

Our data indicate that within a period of 26 days after deafening no detectable reduction of the GDNF-family member expression and their receptors was ascertainable on spiral ganglion cells by immunohistochemistry. Thus, a lack of neurotrophic factor expression is unlikely to be the only cause of spiral ganglion cell loss following deafening.

摘要

背景

最近的研究表明,神经营养因子如脑源性神经营养因子(BDNF)、神经营养素-3(NT-3)和胶质细胞源性神经营养因子(GDNF)在噪声或药物性听力损失后对螺旋神经节细胞具有保护作用。根据这些研究,有人提出耳聋导致螺旋神经节细胞中神经营养因子或相关受体表达缺失,必须通过在耳蜗局部应用这些因子来进行补偿。

方法

在本研究中,我们检测了正常听力和实验性致聋大鼠(10%新霉素)螺旋神经节细胞上GDNF家族成员(GDNF、神经营养因子、Artemin、Persephin)及其相关受体(Ret、GFRalpha1 - 3)以及BDNF和trkB的表达模式。致聋26天后,采用间接免疫荧光法测定这些因子及其受体的蛋白表达。

结果

我们的结果表明,正常听力以及实验性致聋动物的螺旋神经节细胞上存在神经营养因子和受体表达。

结论

我们的数据表明,致聋后26天内,通过免疫组织化学在螺旋神经节细胞上未检测到GDNF家族成员表达及其受体有可检测到的减少。因此,神经营养因子表达缺失不太可能是致聋后螺旋神经节细胞丢失的唯一原因。

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