The role of noradrenaline, dopamine and 5-hydroxytryptamine in the hyperactivity response resulting from the administration of tranylcypramine to rats pretreated with lithium or rubidium.

1. The administration of 15 mg/kg tranylcypromine sulphate (Tc) to rats which have been given lithium chloride (LiCl) in the diet (30 mmol/kg dry food) for 14 days produces hyperactivity within 4 hrs, and this lasts for at least 4 further hours. 2. If LiCl is replaced by rubidium chloride (RbCl) at the same dose, the hyperactivity following Tc is increased and it appears within 2 hrs. 3. 5-Hydroxytryptamine (5HT) accumulation after a monoamine oxidase inhibitor (Tc) is increased 46% and 85% respectively above control values by LiCl and RbCl administration. 4. The hyperactivity produced by the above combinations is inhibited by alpha-methyl-p-tyrosine (alphampt). The inhibition is more effective following LiCl than RbCl treatment. 5. After sodium chloride (NaCl) and LiCl treatment, but not after RbCl treatment, the combination of alphampt and Tc produced rat brain concentrations of dopamine (DA) significantly below control values. 6. The smaller increase of brain noradrenaline (NA) after Tc and RbCl suggests that a lower percentage of NA is being metabolised by MAO. The greater decrease of NA after giving alphampt to RbCl and LiCl treated rats suggests an increased "turnover" rate of Na. 7. The hyperactivity syndrome seen in rats after the administration of LiCl or RbCl and Tc is dependent upon both 5HT and dopamine mechanisms.