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大鼠小脑皮质中神经营养因子受体蛋白免疫反应性随年龄的变化

Neurotrophin receptor proteins immunoreactivity in the rat cerebellar cortex as a function of age.

作者信息

Torres J M, Javier Naves F, Esteban I, Del Valle M E, Vega J A

机构信息

Departamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, Spain.

出版信息

Mech Ageing Dev. 1995 Aug 31;83(1):1-9. doi: 10.1016/0047-6374(95)01616-8.

Abstract

The influence of age on immunohistochemically demonstrable neurotrophin receptor proteins (p75, trkA-, trkB-, and trkC-proteins) was studied in the cerebellar cortex of Wistar male rats aged 3 (young), 12 (adult) and 24 (old) months. The number of Purkinje neurons displaying p75, trkA- and trkC-like proteins immunoreactivity (IR), as well as the intensity of p75 and trkA-like protein IR, were significantly reduced in aged rats in comparison with 3 and 12-month-old rats. The intensity of trkC-like protein in the cytoplasm of Purkinje neurons remained unchanged for all the period studied. Moreover, no significant age-dependent changes were observed in the density of p75 or trkC-like proteins IR in the granule neurons layer. The molecular layer showed faint p75 IR which decreased as a function of age. No immunolabelling for neuronal trkB-like proteins was observed, but trkB- and trkC-like proteins IR was found in non-neuronal cells. These results suggest that cerebellar cortex neurons are responsive to and/or dependent upon different neurotrophins. Moreover, the age-dependent impairment in the expression of some neurotrophin receptors in Purkinje neurons, but not in the granule neurons, lends support to a role for neurotrophins in cerebellar aging.

摘要

研究了年龄对3个月(幼年)、12个月(成年)和24个月(老年)雄性Wistar大鼠小脑皮质中免疫组化可显示的神经营养因子受体蛋白(p75、trkA、trkB和trkC蛋白)的影响。与3个月和12个月大的大鼠相比,老年大鼠中显示p75、trkA和trkC样蛋白免疫反应性(IR)的浦肯野神经元数量,以及p75和trkA样蛋白IR的强度均显著降低。在整个研究期间,浦肯野神经元细胞质中trkC样蛋白的强度保持不变。此外,在颗粒神经元层中,p75或trkC样蛋白IR的密度未观察到明显的年龄依赖性变化。分子层显示微弱的p75 IR,其随年龄增长而降低。未观察到神经元trkB样蛋白的免疫标记,但在非神经元细胞中发现了trkB和trkC样蛋白IR。这些结果表明,小脑皮质神经元对不同的神经营养因子有反应和/或依赖。此外,浦肯野神经元而非颗粒神经元中某些神经营养因子受体表达的年龄依赖性损伤,支持了神经营养因子在小脑衰老中的作用。

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