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The effects of during early life on acetylcholinesterase (AChE) specific activity of , and were examined in rehabilitated adults . Undernourished rats were raised by dams maintained on a scheme from pup birth to pup weaning. The offspring were maintained on a restricted food schedule until day 38 when they started to have free access to food until 70-80 days of age. Control rats were raised by dams which had free access tofood. The results showed that early malnutrition caused a significant increase in AChE specific activity in cerebellum (about 20%), striatum (about 40%), and hypothalamus (about 30%). No changes were found in the hippocampus. Undernutrition caused a significant increase in Vmax when compared to the control group without changes in Km both in cerebellum and striatum. These results suggest that early undernutrition changes AChE concentration in cerebellum and striatum and does not affect the affinity of the enzyme for the substrate.
EN
Using superfusion with albumin-containing medium of hippocampal and striatal slices of adult and developingrats at postnatal days(PND) 7-10, prelabelled with [3H]arachidonic acid ([3H]AA) we detected N-methyl-D-aspartate (NMDA) evoked release to the superfusion medium of radiolabelld material, 70% of which was associated with arachidonic acid (AA) and its metabolite.[3H[AA release was much more pronounced in PND 7-10 rats than in adults, and the response to NMDA in the hippocampal slices exceed the reactions in the striatal slices.The subsequent experiments, emplyoing only hippocampal slices of PND 7-10 rats, demonstrated that NMDA-stimulated [3H]AA release was dose-depended in the micromolar range,was sensitive to NMDA receptor antagonists, and wasinhibited in calcium-free medium and the presence of quinacrine.[3H]AA release induced by 100 ?M NMDA was not significantly inhibited by magnesium but was completly blocked by 7 Cl-kynurenic acid and ifenprodil (both antagonists 100 ?M).The sulfhydryl reducing reagent dithiothreitol induced [3H]AA release; this response was sensitive to NMDA receptor antagonists.These data indicate that the NMDA induced, calcium triggered, and phospholipides A2 depended AA release is highly pronounced in the developing rat hippocampus.NMDA receptors mediating AA release in the hippocampus of PND 7-10 rats are subject to glycine, polyamine and redox modulationn, but they show low sensitivity to Mg2+ inhibition.
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