In vivo effects of a monoamionergic activity enhancer

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: l-DOPA (150–300 mg/kg) after pretreatment with an inhibitor of peripheral l-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100–200 mg/kg); d-amphetamine (1–2 mg/kg); apomorphine (0.25–2.5 mg/kg); lysergic acid diethylamide (100–300 g/kg); and clonidine (0.5–1.0 mg/kg). In contrast β-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with α-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg) or trifluoperazine (5–10 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.