Administration of 6-hydroxydopamine to neonatal rats produces a rapid and profound depletion of brain dopamine. Total activity of treated animals is significantly greater than that of controls between 12 and 22 days of age, but then declines, an activity pattern similar to that seen in affected children. This suggests a functional deficiency of brain dopamine in the pathogenesis of minimal brain dysfunction.

No abstract

We have investigated the relationship between catecholamine turnover and susceptibility to audiogenic seizures (AGS) in the developing DBA/2J mouse. Turnover of dopamine and norepinephrine was determined after administration of alphamethylparatyrosine at 3 weeks of age when nearly all mice (94%) exhibited AGS, at 6 weeks when only 30% were susceptible, and at 12 weeks when none developed seizures. Turnover of brain dopamine increased progressively from 236 ng/g/hr at 3 weeks to 389 ng/g/hr by 12 weeks of age. Norepinephrine turnover increased significantly between 3 and 6 weeks of age, then remained stable thereafter. Turnover times for each catecholamine did not change appreciably with maturation. Our results support the notion that susceptibility to AGS may be mediated in part by brain catecholaminergic mechanisms.