Abstract：
Exposure to light has been demonstrated to stimulate brain regions associated with cognition; however, investigations into its cognitive-enhancing effects have primarily focused on wild-type rodents. This study seeks to elucidate how bright light exposure mitigates cognitive deficits associated with schizophrenia by examining its impact on hippocampal neurogenesis and its potential to alleviate sub-chronic MK-801-induced cognitive impairments in mice. Following three weeks of juvenile bright light exposure (5-8 weeks old), significant increases in proliferating neurons (BrdU+) and immature neurons (DCX+ cells) were observed in the dentate gyrus (DG) and lateral ventricle of MK-801-treated mice. Long-term bright light treatment further promoted the differentiation of BrdU+ cells into immature neurons (BrdU+ DCX+ cells), mature neurons (BrdU+ NeuN+ cells), or astrocytes (BrdU+ GFAP+ cells) in the hippocampal DG. This augmented neurogenesis correlated with the attenuation of sub-chronic MK- 801-induced cognitive deficits, as evidenced by enhancements in Y-maze, novel object recognition (NOR), novel location recognition (NLR), and Morris water maze (MWM) test performances. These findings suggest a promising noninvasive clinical approach for alleviating cognitive impairments associated with neuropsychiatric disorders.
摘要：
已证明暴露于光刺激与认知相关的大脑区域;然而，对其认知增强作用的研究主要集中在野生型啮齿动物。这项研究旨在通过研究强光暴露对海马神经发生的影响及其减轻小鼠亚慢性MK-801诱导的认知障碍的潜力来阐明强光暴露如何减轻与精神分裂症相关的认知障碍。经过三周的青少年强光照射（5-8周大），在MK-801处理的小鼠的齿状回（DG）和侧脑室中观察到增殖神经元（BrdU）和未成熟神经元（DCX细胞）的显着增加。长期强光处理进一步促进了BrdU+细胞向未成熟神经元（BrdU+DCX+细胞）的分化，成熟神经元（BrdU+NeuN+细胞），或海马DG中的星形胶质细胞(BrdU+GFAP+细胞)。这种增强的神经发生与亚慢性MK-801诱导的认知缺陷的衰减相关，Y迷宫的增强证明了这一点，新颖的对象识别(NOR)，新颖的位置识别(NLR)，和Morris水迷宫(MWM)测试性能。这些发现表明了一种有希望的非侵入性临床方法来减轻与神经精神疾病相关的认知障碍。
