Cues intrinsic to the retina induce nAChR gene expression during development.

Cues intrinsic to the retina induce nAChR gene expression during development.
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视网膜固有的信号在发育过程中诱导 nAChR 基因表达。

DOI:
10.1002/neu.480240808
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发表时间:
1993
期刊:
Journal of neurobiology
影响因子:
--
通讯作者:
Goldman,D
Goldman,D
中科院分区:
--
文献类型:
--
作者:
Hankin,MH;Hoover,F;Goldman,D

文献摘要

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最近对金鱼视神经再生的研究表明,视神经顶盖在视网膜神经节细胞再生过程中调节烟碱乙酰胆碱受体(nAChR)基因表达诱导中起重要作用(Hieber, Agranoff, and Goldman, 1992,J。neurochem.58:1009 - 1015)。这些观察结果表明,这些基因的诱导是由大脑靶区调节的。发育中的大鼠视网膜中nAChR mRNA的出现与神经节细胞向其大脑目标发送轴突的时间一致(Hoover and Goldman, 1992,Exp。眼睛res.54:561 - 571)。在哺乳动物视网膜发育过程中,是否也有类似于金鱼视神经再生过程中的机制介导nAChR基因的表达?通过将胚胎大鼠视网膜移植到不同的脑区,或将其移植到器官培养中并检测nAChR基因的表达来验证这种可能性。这些研究表明,nAChR基因在发育中的大鼠视网膜中的诱导与视网膜发育的环境无关。这些结果表明,视网膜微环境或视网膜神经节细胞固有的信号是这种诱导的原因。©1993 John Wiley & Sons, Inc
Recent studies of optic nerve regeneration in goldfish have indicated that the optic tectum plays an important role in modulating the induction of nicotinic acetylcholine receptor (nAChR) gene expression in regenerating retinal ganglion cells (Hieber, Agranoff, and Goldman, 1992,J. Neurochem.58:1009–1015). These observations suggest that induction of these genes is regulated by brain target regions. The appearance of nAChR mRNA in the developing rat retina coincides with a time when ganglion cells are sending axons to their brain targets (Hoover and Goldman, 1992,Exp. Eye Res.54:561–571). Might a mechanism similar to that seen during goldfish optic nerve regenerationalso mediate induction of nAChR gene expression during development of the mammalian retina? This possibility was tested by either transplanting embryonic rat retina to different brain regions, or explanting it to organ culture and assaying for nAChR gene expression. These studies showed that induction of the nAChR genes in developing rat retina is independent of the environment in which the retina develops. These results indicate that either the retinal microenvironment or a signal intrinsic to the retinal ganglion cell is responsible for this induction. © 1993 John Wiley & Sons, Inc.