Pardal J F
J Neurosci Res. 1980;5(2):155-61. doi: 10.1002/jnr.490050207.
Action of dextro-phenylalanine (d-Phe) on catecholamine release elicited by K+20 mM has been studied in isolated slices of rat central nervous system (CNS). d-Phe (3 x 10(-3)M) produced inhibition of the fractional release of 3H-noradrenaline but not of 3H-dopamine. The mentioned effect is Ca2+ dependent and was antagonized when this ion was incremented to 2.6 mM in the medium or in the presence of ionophore A-23187 (4 x 10(-5)M). Neither acetylsalicylic acid nor indomethacin (prostaglandin biosynthesis inhibitors) interferes with the effect of d-Phe, showing that by itself it would not reach through the prostaglandin pathway. d-Phe modified neither the noradrenaline neuronal uptake nor its metabolism at the CNS. The findings suggest that d-Phe acts through a Ca2+-dependent mechanism, possibly by specific receptors and in parallel with feedback circuits that involve alpha-adrenoceptors, muscarinic receptors, or prostaglandins.
已在大鼠中枢神经系统（CNS）离体切片中研究了右旋苯丙氨酸（d-Phe）对20 mM K⁺引发的儿茶酚胺释放的作用。d-Phe（3×10⁻³M）抑制了³H-去甲肾上腺素的分数释放，但未抑制³H-多巴胺的释放。上述作用依赖于Ca²⁺，当培养基中该离子浓度增加到2.6 mM或存在离子载体A-23187（4×10⁻⁵M）时，这种作用会被拮抗。乙酰水杨酸和吲哚美辛（前列腺素生物合成抑制剂）均不干扰d-Phe的作用，表明其本身不会通过前列腺素途径发挥作用。d-Phe既不改变去甲肾上腺素在中枢神经系统的神经元摄取，也不改变其代谢。这些发现表明，d-Phe通过一种依赖于Ca²⁺的机制发挥作用，可能是通过特定受体，并与涉及α-肾上腺素能受体、毒蕈碱受体或前列腺素的反馈回路并行发挥作用。
