Juorio A V, Boulton A A
J Neurochem. 1982 Sep;39(3):859-63. doi: 10.1111/j.1471-4159.1982.tb07971.x.
The parenteral administration of L-phenylalanine or p-tyrosine increases the mouse striatal concentration of p-tyramine, an effect that is enhanced by monoamine oxidase inhibition and reduced by an L-aromatic aminoacid decarboxylase inhibitor. Striatal m-tyramine was increased following administration of L-phenylalanine or m-tyrosine and enhanced further by monoamine oxidase inhibition. It was also observed that m-tyrosine is a better substrate for decarboxylation than p-tyrosine, and that p-tyrosine decarboxylation was blocked by NSD 1055, while that of m-tyrosine was enhanced. The results obtained indicate that both isomers of tyramine are formed in the mouse striatum by hydroxylation of L-phenylalanine to p- or m-tyrosine followed by decarboxylation by a specific decarboxylase; an alternative pathway could be first the decarboxylation of phenylalanine to beta-phenylethylamine, followed by its hydroxylation to p- or m-tyramine.
经肠胃外途径给予L-苯丙氨酸或对酪氨酸会增加小鼠纹状体中对酪胺的浓度，单胺氧化酶抑制可增强此效应，而L-芳香族氨基酸脱羧酶抑制剂则可减弱该效应。给予L-苯丙氨酸或间酪氨酸后，纹状体中的间酪胺增加，单胺氧化酶抑制可使其进一步增加。还观察到，间酪氨酸比酪氨酸是更好的脱羧底物，对酪氨酸的脱羧被NSD 1055阻断，而间酪氨酸的脱羧则增强。所得结果表明，酪胺的两种异构体在小鼠纹状体中通过L-苯丙氨酸羟基化为对或间酪氨酸，然后由特定脱羧酶进行脱羧而形成；另一种途径可能是首先将苯丙氨酸脱羧为β-苯乙胺，然后将其羟基化为对或间酪胺。
