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Age-related changes in neurochemical components and retinal projections of rat intergeniculate leaflet

机译:大鼠种间小叶神经化学成分和视网膜投射的年龄相关变化

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摘要

Aging leads to several anatomical and functional deficits in circadian timing system. In previous works, we observed morphological alterations with age in hypothalamic suprachiasmatic nuclei, one central component of this system. However, there are few data regarding aging effects on other central components of this system, such as thalamic intergeniculate leaflet (IGL). In this context, we studied possible age-related alterations in neurochemical components and retinal projections of rat IGL. For this goal, young (3 months), adult (13 months), and aged (23 months) Wistar rats were submitted to an intraocular injection of neural tracer, cholera toxin subunit b (CTb), 5 days before a tissue fixation process by paraformaldehyde perfusion. Optical density measurements and cell count were performed at digital pictures of brain tissue slices processed by immunostaining for glutamic acid decarboxylase (GAD), enkephalin (ENK), neuropeptide Y (NPY) and CTb, characteristic markers of IGL and its retinal terminals. We found a significant age-related loss in NPY immunoreactive neurons, but not in immunoreactivity to GAD and ENK. We also found a decline of retinal projections to IGL with age. We conclude aging impairs both a photic environmental clue afferent to IGL and a neurochemical expression which has an important modulatory circadian function, providing strong anatomical correlates to functional deficits of the aged biological clock.
机译:老化会导致昼夜节律计时系统出现一些解剖和功能缺陷。在以前的工作中,我们观察到了下丘脑上裂眼上核(该系统的重要组成部分)随年龄的形态变化。但是,很少有关于老化对该系统其他中央组件(例如丘脑间质小叶(IGL))的数据。在这种情况下,我们研究了大鼠IGL的神经化学成分和视网膜投影可能与年龄有关的变化。为了这个目标,在组织固定过程前5天,将年轻的(3个月),成年的(13个月)和年长的(23个月)Wistar大鼠进行眼内注射神经示踪剂霍乱毒素亚基b(CTb)。多聚甲醛灌注。在通过对谷氨酸脱羧酶(GAD),脑啡肽(ENK),神经肽Y(NPY)和CTb进行免疫染色处理的脑组织切片的数码照片上进行光密度测量和细胞计数,这是IGL及其视网膜末端的特征标记。我们发现NPY免疫反应性神经元与年龄有关的明显丧失,但GAD和ENK的免疫反应性却没有。我们还发现,随着年龄的增长,对IGL的视网膜预测会下降。我们得出结论,衰老会损害IGL传入的光化学环境线索以及具有重要的调节性昼夜节律功能的神经化学表达,从而为衰老的生物钟的功能缺陷提供强大的解剖学关联。

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