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EFFECT OF AMANTADINE ON THE RATE OF DOPAMINE SYNTHESIS IN RAT CORPUS STRIATUM 1
Author(s) -
Bariletto S.,
Dollar Elizabeth,
Leitz F.
Publication year - 1975
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1975.tb12240.x
Subject(s) - homovanillic acid , dopamine , amantadine , striatum , apomorphine , chemistry , endocrinology , medicine , haloperidol , endogeny , metabolite , tyrosine , dopaminergic , pharmacology , biology , biochemistry , serotonin , receptor
— The effect of amantadine on the rate of dopamine synthesis in rat corpus striatum was determined by three methods. (1) Measuring the rate of decline of endogenous dopamine following inhibition of synthesis with a‐methyltyrosine (α‐MT); (2) Measuring the rate of conversion of [3,5‐ 3 H]tyrosine to 3 H‐labelled catechols under conditions of an initial rate; and (3) measuring the levels of homovanillic acid (HVA), the principal metabolite of brain dopamine. Endogenous dopamine levels were 68‐1 n‐mole/g with a control synthesis rate of about 21 n‐mole/g/h as determined using either α‐MT or [3,5‐ 3 H]tyrosine. Amantadine had no effect on synthesis at doses up to 100 mg/kg using α‐MT and [3,5‐ 3 H]tyrosine. HVA levels were unaffected after 30 mg/kg drug, but were elevated 48% (P < 005) after 100 mg/kg of drug. By contrast apomorphine reduced and haloperidol increased synthesis as determined by all three methods. It is concluded that amantadine has no marked effect on dopamine synthesis in rat corpus striatum.