目的：该文旨在了解高苯丙氨酸(Phe)对大脑皮层神经元Nogo 66 受体(NgR)表达的影响，以探讨NgR是否参与高Phe脑损伤的发病。方法：采取体外模拟高Phe（0.9 mM）环境，原代培养胎龄16~18 d的SD胎鼠皮层神经元，用免疫荧光方法观察高Phe作用0 h，12 h，24 h之后神经元轴突长度和生长锥塌陷情况，并用实时荧光定量PCR和Western blot方法检测高Phe作用0 h，12 h，24 h和48 h NgR mRNA和蛋白的表达情况。结果：①高Phe作用12 h，24 h组神经元轴突长度与对照组相比明显变短（均P<0.05），0 h，12 h和24 h生长锥塌陷比率分别为（3.5±1.5）%，（12.5±9.7）%和（24.1±4.5）%，12 h组和24 h 组与对照组（0 h组）相比，生长锥塌陷明显增多（P<0.01）；②荧光定量PCR检测到高Phe作用12 h，24 h，48 h神经元NgR mRNA与alpha-tubulin (α-Tub，α微管蛋白)的相对表达量轻度升高，但Ct值差异无显著性；③Western-blot 检测发现高Phe作用12 h，24 h和48 h的神经元NgR蛋白明显增加，12 h，24 h和48 h组的相对比值分别为对照组的9.0，9.4，12.6倍（P<0.05）。结论：高Phe可使神经元NgR受体表达增高，其可能为高Phe导致脑损伤神经元生长锥塌陷、突起生长减慢的机制之一。

OBJECTIVE: This study examined the effect of high concentration of phenylalanine (Phe) on Nogo-66 receptor (NgR) expression in the cortical neurons of rats in vitro in order to investigate whether NgR is involved in the etiology of Phe-induced brain damage. METHODS: Neurons from the cerebral cortex of embryonic rats were cultured for 3 days and then were treated with 0.9 mM Phe. After 12, 24 and 48 hrs of Phe treatment, mRNA and protein expression of NgR was detected by real-time PCR and Western blot respectively. Growth cones and growth axons of neurons were detected by immunofluorescence and immunohistochemistry respectively after 12 and 24 hrs of Phe treatment. RESULTS: The length of growth axons of neurons was significantly shorter after 12 and 24 hrs of Phe treatment compared with the control group without Phe treatment (P<0.05). Growth cones collapse occurred in 12.5±9.7% and 24.1±4.5% of neurons respectively after 12 and 24 hrs of Phe treatment but only in 3.5±1.5% in the control group (P<0.01). The protein level of NgR after 12, 24 and 48 hrs of Phe treatment was up-regulated, with 9.0, 9.4 and 12.6 times as the control. mRNA level of NgR in the Phe treatment group did not differ from control. CONCLUSIONS: High concentration of Phe can induce an increased NgR protein expression in cortical neurons, and the increased NgR expression may contribute to the growth cones collapse and the inhibitory activities of axon regeneration after injury.