Delays in growth and biochemical development of rat brain caused by maternal methadone administration: are the alterations in synaptogenesis and cellular maturation independent of reduced maternal food intake?
Food consumption of control pregnant and nursing rats was matched to that of methadone-treated dams and the patterns of growth and of biochemical development of the brain in the offspring were compared, using tyrosine hydroxylase activity as a marker for synaptogenesis of catecholamine neurons and the developmental pattern of ornithine decarboxylase activity as an index of delay of cellular maturation. Although body growth was slowed significantly, the degree of deficit was attenuated compared to previously reported experiments with non-pair-fed controls. Reduced brain weight and slowing of synaptogenesis also were evident in the methadone-exposed pups, and in this case, the effect was not attenuated with the use of pair-fed controls. Reduced brain weight and slowing of synaptogenesis also were evident in the methadone-exposed pups, and in this case, the effect was not attenuated with the use of pair-fed controls. Delays in the normal maturational decline of brain ornithine decarboxylase activity were prominent in the methadone group compared to offspring of pair-fed controls, just as reported previously in comparisons using non-pair-fed dams. These results indicate the part of the general growth deficit seen in perinatally-addicted pups is related to maternal undernutrition, but that delays in central synaptogenesis or in the pattern of biochemical maturation of the brain are relatively independent of the nutritional deficit.
Seidler, FJ; Whitmore, WL; Slotkin, TA
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