The role of the catecholaminergic system in foot shock-induced fighting aggression in mice was studied with the help of behavioral tests and biochemical experiments. The administration of the catecholamine precursor l-dopa combined with enzymatic decomposition inhibitors (nialamide or Ro4-4602) produced a significant increase in the number of fighting episodes in mice. The administration of the dopamine agonists amantadine, apomorphine, and nomifensine also increased aggression in mice. Catecholamine synthesis inhibitors, alpha-MT and compounds blocking catecholamines receptors (pimozide and haloperidol), reduced the number of fighting epidoses in mice. Clonidine, a noradrenergic agonist, potentiated the aggressive behavior of mice while the noradrenergic antagonists aceperone and phenoxybenzamine, the alpha-adrenergic receptor blockers, suppressed aggression. The noradrenaline synthesis inhibitor FLA-63 also depressed the number of fighting episodes in mice. A comparison of two effective doses (ED50) for antiaggressive action and for the inhibition of motor activity showed that alpha-MT, FLA-63, and aceperone reduced the number of fighting episodes in mice most selectively. The interaction between catecholamine agonists and antagonists showed that an increase of aggression induced by nialamide plus l-dopa was abolished both by haloperidol and by phenoxybenzamine. Clonidine effects were also partially weakened by phenoxybenzamine. Studies on noradrenaline and dopamine levels in the brains of mice, after the synthesis of those catecholamines was inhibited, showed a higher noradrenaline utilization in the brains of aggressive mice than in nonaggressive mice. The present results suggest a significant role of noradrenaline dopamine in producing the foot shock-induced fighting aggression in mice.
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