Cerebral decarboxylation of meta- and para-tyrosine.
The decarboxylase inhibitor DL-alpha-monofluoromethyldopa reduces, in a dose dependent manner, the concentration of striatal p-tyramine in the mouse. Homovanillic acid is also significantly reduced. Conversely, this treatment increases the m-tyramine concentration. Administration of m-tyrosine produces large increases in m-tyramine and a slight decrease in p-tyramine; these changes are potentiated in the presence of the decarboxylase inhibitor. Such data along with other recently published results permit the conclusion that m-tyramine arises from phenylalanine via m-tyrosine and that p-tyramine arises by decarboxylation of p-tyrosine. Both these reactions are closely related to the activity of tyrosine hydroxylase and the availability of appropriate substrates.
D000818:Animals; D002262:Carboxy-Lyases / Q000037:antagonists & inhibitors; D003342:Corpus Striatum / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D008750:Methyldopa / Q000031:analogs & derivatives* / Q000494:pharmacology; D051379:Mice; D014439:Tyramine / Q000378:metabolism; D014443:Tyrosine / Q000378:metabolism* / Q000494:pharmacology
D014443:Tyrosine; D008750:Methyldopa; C019494:alpha-monofluoromethyldopa; C015566:3-tyrosine; D002262:Carboxy-Lyases; C028169:3-tyramine; D006719:Homovanillic Acid; D014439:Tyramine