Alphamethyl-p-tyrosine (a-MT) inhibits brain tyrosinehydroxylase activity but has only small effects on tryptophanehydroxylase [13]. The substance has been used clinically in attempts to reduce cateeholaminergic activity [4,5,8]. The levels of amine metabolites in eerebrospinal fluid (CSF) have been determined in several neuropsyehiatric conditions in an attempt to evaluate the monoaminergic activity in the central nervous system (For review: see [10]). The results of animal studies indicate that the turnover of amines in the brain and the concentrations of their metabolites in CSF are correlated [6].
Probeneeid inhibits a transport system carrying monoamine acids from CSF to blood [9,7]. After administration of probenecid, an increase of the concentration of the acids in CSF has been found [11]. The rate of increase is conceivably proportional to the activity in the neurons. Probeneeid-loading makes it thus possible to estimate turnover and release in central monoaminergic neurons in man. It has been shown [2] that ~-MT reduces the concentration of homovanillic acid (ttVA) in CSF of cats and prevents the rise of I=[VA after probenecid. The aim of the present investigation was to study the effects of a-MT on HVA and 5-hydroxyindoleaeetic acid (5-HIAA) in CSF in man with and without probeneeid-applieation.