Sadava D, Sutcliffe D
Joint Science Department, Claremont Colleges, California 91711.
Life Sci. 1988;43(14):1119-23. doi: 10.1016/0024-3205(88)90470-5.
Pregnant rats were given a diet supplemented with 0.5% alpha-methyl-phenylalanine and 3% phenylalanine from the 12th day of gestation to term. Compared to unsupplemented controls, maternal serum phenylalanine was elevated 8-10-fold. Experimental litters did not differ from controls in number of offspring, birth weight, or subsequent growth on an unsupplemented diet. At 8 weeks of age, animals were tested for latent learning on a 4-arm maze, and at 10 weeks, they were tested for observational learning with littermates in a food preference paradigm. In both tests, experimental animals did learn, but significantly less than controls. The data suggest that maternal hyperphenylalaninemia, induced as a model for the inborn error, phenylketonuria, can lead to learning deficits later in the lives of offspring.
从妊娠第12天到足月,给怀孕的大鼠喂食添加了0.5%α-甲基苯丙氨酸和3%苯丙氨酸的饮食。与未添加饮食的对照组相比,母体血清苯丙氨酸升高了8至10倍。实验窝仔在后代数量、出生体重或未添加饮食后的后续生长方面与对照组没有差异。在8周龄时,对动物进行四臂迷宫潜在学习测试,在10周龄时,在食物偏好范式中与同窝仔进行观察学习测试。在两项测试中,实验动物确实有学习,但明显少于对照组。数据表明,作为先天性代谢缺陷苯丙酮尿症模型诱发的母体高苯丙氨酸血症,可导致后代后期出现学习缺陷。