Neurobehavioural deficits following postnatal iron overload: I spontaneous motor activity.

摘要: Five experiments that induced postnatal iron overload in mice are described. In Experiment I, exposure of NMRI to different doses (iron succinate: 0.0, 3.7 or 37.0 mg Fe2+/kg b. w., p.o.) on days (PD) 10—PD12 indicated marked disruptions spontaneous motor behaviour and habituation the dose group, a lesser extent group. Analysis brain content significantly more total (μg/g) basal ganglia, but not frontal cortex higher, 37 mg/kg, II, newborn were administered Fe2+ (7.5 b.w.) at either PD 3–5, 10–12 19–21, vehicle (saline). Marked deficits obtained during 10–12, much 3–5. (mg/g) from 3–5 treatment groups. III, interactive effects administration 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) adult C57 BL/6 examined by (Fe2+) 7.5 wt., p.o. (saline) followed, 3-months age, MPTP (2 × 20 2 40 s.c.) saline. Postnatal mg/kg) caused drastic activity behavioural testing (4-months age), potentiated these disruptions. Neurochemical dopamine (DA) its metabolites (dihydroxyphenylacetic acid, DOPAC; homovanillic HVA) exacerbated prior Fe2+. The analysis regions notably elevated levels 10–12. MPTP-treated displayed severe depletions DA, DOPAC HVA both striatal cortical regions, i.e. Veh-MPTP40 as well Fe-MPTP20 Fe-MPTP40 groups, compared saline-treated (Vehicle) 4-months with Veh-MPTP20 IV it was (hypoactivity), initially, all three parameters 5.0 mg/kg doses, 2.5 dose. Later combination severely deficits. During final period hyperactivity for two higher groups; this effect abolished MPTP. V, iron-induced alleviated dose-related manner co-administration uncompetitive glutamate receptor antagonist, dizolcipine (MK-801), subthreshold L-Dopa. Iron-overload immediate seems detrimental several aspects functional neurobiological development.