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脉络膜血流神经调节中断后视网膜病理变化的证据:在鸽子中,动眼神经核损伤后 Müller 细胞表达胶质纤维酸性蛋白。

Evidence for retinal pathology following interruption of neural regulation of choroidal blood flow: Müller cells express GFAP following lesions of the nucleus of Edinger-Westphal in pigeons.

作者信息

Fitzgerald M E, Vana B A, Reiner A

机构信息

Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN 38163.

出版信息

Curr Eye Res. 1990 Jun;9(6):583-98. doi: 10.3109/02713689008999598.

DOI:10.3109/02713689008999598
PMID:2201485
Abstract

Choroidal blood flow in pigeons is regulated by the medial part of the nucleus of Edinger-Westphal (EW) via the ipsilateral ciliary ganglion. Interruption of this circuit by unilateral lesions of EW results in pathological modifications in the morphology of retinal photoreceptors in the ipsilateral eye in pigeons housed under 12hr light (400 lux)/12hr dark conditions. In the present study, we examined the effects of unilateral EW lesions on glial fibrillary acidic protein (GFAP) expression by retinal Müller cells in pigeons housed under the same lighting conditions. Since Müller cells in the retina of land vertebrates express increased GFAP during conditions of retinal pathology or stress (e.g. inflammation or hypoxia), this study would enable us to further evaluate the effects of disruption in the neural regulation of choroidal blood flow on the retina. We found that following EW lesions, retinal Müller cells expressed GFAP, with the precise intracellular location of the GFAP dependent on the amount of time elapsed following the lesion. One week after the EW lesions, GFAP labelling was restricted to the Müller cell endfeet in the nerve fiber layer and ganglion cell layer. By two-three weeks, the labelling had extended outward (or sclerad) into the portions of the Müller cells spanning the inner plexiform layer. Finally, by six weeks post-lesion, the entire extent of the Müller cell from the nerve fiber layer to the outer limiting membrane contained GFAP. No GFAP immunoreactivity in Müller cells was observed in the eyes contralateral to the EW lesions or in eyes in which the pupil had been fixed and dilated by lesions of the pretectal region. Our results suggest that the retina is in a state of physiological stress following interruption of the neural regulation of choroidal blood flow by EW lesions. Although the precise mechanisms by which altered choroidal blood flow regulation affects Müller cell GFAP production require elucidation, the results nonetheless highlight the importance of intact neural regulation of choroidal blood flow for retinal health.

摘要

家鸽脉络膜血流受动眼神经核(EW)内侧部分通过同侧睫状神经节调节。在12小时光照(400勒克斯)/12小时黑暗条件下饲养的家鸽中,EW单侧损伤中断该回路会导致同侧眼视网膜光感受器形态发生病理改变。在本研究中,我们检测了在相同光照条件下饲养的家鸽中,EW单侧损伤对视网膜Müller细胞胶质纤维酸性蛋白(GFAP)表达的影响。由于陆地脊椎动物视网膜中的Müller细胞在视网膜病理或应激状态(如炎症或缺氧)下GFAP表达增加,本研究将使我们能够进一步评估脉络膜血流神经调节中断对视网膜的影响。我们发现,EW损伤后,视网膜Müller细胞表达GFAP,GFAP在细胞内的确切位置取决于损伤后经过的时间。EW损伤一周后,GFAP标记仅限于神经纤维层和神经节细胞层的Müller细胞终足。到两到三周时,标记已向外(或向巩膜侧)扩展到跨越内丛状层的Müller细胞部分。最后,在损伤后六周时,从神经纤维层到外界膜的整个Müller细胞范围都含有GFAP。在EW损伤对侧的眼睛或顶盖前区损伤导致瞳孔固定和散大的眼睛中,未观察到Müller细胞的GFAP免疫反应性。我们的结果表明,EW损伤中断脉络膜血流神经调节后,视网膜处于生理应激状态。尽管脉络膜血流调节改变影响Müller细胞GFAP产生的确切机制尚需阐明,但结果仍然突出了脉络膜血流完整神经调节对视网膜健康的重要性。

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