Laskowska-Macios Karolina, Arckens Lutgarde, Kossut Małgorzata, Burnat Kalina
Laboratory of Neuroplasticity, Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland; Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Leuven, Belgium.
Laboratory of Neuroplasticity and Neuroproteomics, KU Leuven, Leuven, Belgium.
Acta Neurobiol Exp (Wars). 2017;77(3):199-204. doi: 10.21307/ane-2017-053.
Deprivation of patterned visual information, as in early onset congenital cataract patients, results in a severe impairment in global motion 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 corroborate these 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-related BDNF expression we compared the central and the peripheral visual field representations of area 17 of 1, 2, 4 and 6-month-old and adult 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 months of normal vision (2N2BD), as animal models of congenital and delayed onset cataract. During normal cortical development the BDNF transcript levels, measured by quantitative RT-PCR, remained stable. Higher BDNF mRNA levels were found in central area 17 of 2BD and 6BD animals compared to age-matched controls. In central area 17, the high BDNF mRNA levels at the end of the BD period may activate a mechanism by which plastic processes, halted by deprivation, may begin. We here confirm that the peripheral visual field representation of area 17 matures slower than its central counterpart. Only in central area 17 normal visual input upon BD could upregulate BDNF mRNA which may lead to a fast activation of local plastic adaptations.
如在早发性先天性白内障患者中那样,剥夺有模式的视觉信息会导致全局运动感知严重受损。此前我们基于二维差异凝胶电泳筛选蛋白质表达变化以及对活性报告基因ZIF268进行原位杂交,报告了初级视区17中周边视野表征的延迟成熟。为了证实这些发现,我们在此探究脑源性神经营养因子(BDNF)的双眼模式剥夺(BD)调节表达,BDNF是一种已被充分描述的神经营养因子,其表达受早期视觉经验急剧调节。为了评估与成熟相关的BDNF表达的时间,我们比较了在正常视觉条件下饲养的1、2、4和6月龄以及成年猫的视区17的中央和周边视野表征。为了仔细研究BD的结果,比较了四种不同的剥夺策略,包括从出生开始并持续2、4或6个月的早发性BD(2BD、4BD、6BD),以及在正常视觉2个月后进行2个月的迟发性BD(2N2BD),作为先天性和迟发性白内障的动物模型。在正常皮质发育过程中,通过定量逆转录-聚合酶链反应测量的BDNF转录水平保持稳定。与年龄匹配的对照组相比,在2BD和6BD动物的中央视区17中发现了更高的BDNF mRNA水平。在视区17的中央区域,BD期结束时的高BDNF mRNA水平可能会激活一种机制,通过该机制,因剥夺而停止的可塑性过程可能会开始。我们在此证实,视区17的周边视野表征比其中央对应物成熟得更慢。只有在视区17的中央区域,BD后的正常视觉输入才能上调BDNF mRNA,这可能导致局部可塑性适应的快速激活。