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首页> 外文期刊>Acta neurobiologiae experimentalis >BDNF expression in cat striate cortex is regulated by binocular pattern deprivation
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BDNF expression in cat striate cortex is regulated by binocular pattern deprivation

机译:猫双眼纹剥夺调节猫纹状体皮质中的BDNF表达

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摘要

Deprivation of patterned visual information, as in early onset congenital cataract patients, results in a severe impairment in globalmotion perception. Previously we reported a delayed maturation of the peripheral visual field representation in primary visual area 17,based on a 2?D DIGE screen for protein expression changes and in situ hybridization for the activity reporter gene ZIF268. To corroboratethese findings we here explore the binocular pattern deprivation (BD)?regulated expression of brain?derived neurotrophic factor(BDNF), a well?described neurotrophin precipitously regulated by early visual experience. To assess the timing of maturation?relatedBDNF expression we compared the central and the peripheral visual field representations of area 17 of 1, 2, 4 and 6?month?old andadult cats reared under normal visual conditions. To scrutinize the outcome of BD, four different deprivation strategies were compared,including early onset BD from birth and lasting for 2, 4 or 6 months (2BD, 4BD, 6BD), and late onset BD for 2 months upon 2 monthsof normal vision (2N2BD), as animal models of congenital and delayed onset cataract. During normal cortical development the BDNFtranscript levels, measured by quantitative RT?PCR, remained stable. Higher BDNF mRNA levels were found in central area 17 of 2BDand 6BD animals compared to age?matched controls. In central area 17, the high BDNF mRNA levels at the end of the BD period mayactivate a mechanism by which plastic processes, halted by deprivation, may begin. We here confirm that the peripheral visual fieldrepresentation of area 17 matures slower than its central counterpart. Only in central area 17 normal visual input upon BD couldupregulate BDNF mRNA which may lead to a fast activation of local plastic adaptations.
机译:像早期发作的先天性白内障患者一样,缺乏图案化的视觉信息会导致整体运动知觉严重受损。以前我们报道了基于2D DIGE筛选蛋白质表达变化和活性报告基因ZIF268的原位杂交的初级视野17中外围视野表示的延迟成熟。为了证实这些发现,我们在这里探索了由双眼模式剥夺(BD)调节的脑源性神经营养因子(BDNF)的表达,这是一种由早期视觉经验来严格调节的神经营养蛋白。为了评估与成熟相关的BDNF表达的时机,我们比较了在正常视觉条件下饲养的1、2、4和6个月大的成年猫的区域17的中央和周围视野。为了详细研究BD的结局,比较了四种不同的剥夺策略,包括从出生到出生并持续2、4或6个月(2BD,4BD,6BD)的早期BD发作,以及正常视力2个月后2个月的BD晚期发作( 2N2BD),作为先天性和迟发性白内障的动物模型。在正常的皮质发育过程中,通过定量RT?PCR测定的BDNF转录水平保持稳定。与年龄匹配的对照组相比,在2BD和6BD动物的中心区域17发现更高的BDNF mRNA水平。在中心区域17,BD时期结束时高的BDNF mRNA水平可能激活了一种机制,通过该机制可以开始因剥夺而停止的塑性过程。我们在这里确认,区域17的外围视野表示比其中心对应区域慢。仅在BD的中心区域17中,正常的视觉输入可以上调BDNF mRNA,这可能导致局部塑性适应的快速激活。

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