α-Methyl-DOPA was injected into rats in repeated doses to ensure a strong accumulation of α-methyl-noradrenaline in in central noradrenaline storing neurons. Using a histochemical fluorescence method the release of α-methyl-noradrenaline from these neurons could be demonstrated after treatment with the following drug combinations, a) desipramine or protriptyline combined with tetrabenazine or reserpine and b) (+)-amphetamine combined with tetrabenazine or reserpine. None of the drugs when given alone was capable of reducing the fluorescence observed at the interval studied. The release obtained was accompanied by behavioural activation, suggesting that α-methyl-noradrenaline may act as a ‘false transmitter’ in the brain. Inhibition of the first step in the catecholamine biosynthesis was found to reduce t this behavioural activation, however, suggesting that endogenous noradrenaline was of primary importance for the behavioural syndrome. Furthermore, the data suggest that α-methyl-dopamine present in dopamine nerve terminals can be released by (+)-amphetamine but not by desipramine.