Pregnant rats were exposed to drinking water with lead (Pb) concentrations of 0, 30, or 200 mg/l. The resultant pups were sacrificed at 11, 15, and 21 d of postnatal age for the determination of synapses/mm3 in parietal cortex. Synaptic counts from electron micrographs of ethanol phosphotungstic acid stained cortical slices were counted by four observers who were blinded as to treatment (control or 200 mg Pb/l drinking water). A greater than fourfold increase in synaptic counts was observed in layers I, II, and III of rat pups parietal cortex between 11 and 21 d of age. Pb treatment depressed synaptic counts maximally at 15 d of age. However, Pb-exposed pups displayed essentially the same synaptic counts as controls by 21 d of age. In a cross-fostering design, it was shown that prenatal exposure to Pb completely accounted for the delays in synaptogenesis. No significant depression of synaptic counts was observed in pups exposed only during the postnatal period. Blood lead concentrations (Pb X B) were determined during gestation and suckling in both mother and offspring. A dramatic peripartum (partum plus and minus 4 d) peak in Pb X B was seen in mother and pup. Pup Pb X B peaked at 80 micrograms/dl at exposures of 200 mg Pb/l drinking water. In addition to being dose-dependent, blood Pb levels resulting from the same concentration of Pb in drinking water displayed a significant dependence on litter at time-points between birth and 1 yr of age. These data indicate that the substantially elevated blood Pb concentrations that are evident at partum in pups prenatally exposed to Pb might be responsible for the postnatally observed delay in synaptogenesis.

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Abstract— The initial effects of an elevated potassium concentration (30 mm) on the energy metabolism of incubated slices of rat cerebral cortex have been examined using spectrophotometric and polarographic techniques. Respiratory responses to additions of potassium were found to be definitely limited in time. This response was followed by an increase in the rate of aerobic glycolysis. Slice NAD(P)H and cytochrome b paralleled this metabolic sequence by exhibiting an initial oxidation followed by a net increase in the steady‐state levels of reduced intermediates, particularly in the case of NAD(P)H. Substitution of pyruvate (10 mm) for glucose in the standard incubation media produced significant alterations in the respiratory responses to the addition of potassium. Although the period of increased oxygen consumption was again limited it was somewhat greater in magnitude and significantly prolonged in time relative to changes observed with glucose as substrate. Changes in steady‐state levels of NAD(P)H were altered similarly and the net increase of NAD(P)H was not observed with pyruvate as substrate. We suggest that the metabolic responses of brain slices to increased potassium do not involve simultaneous activation of the respiratory and glycolytic pathways as has been previously assumed. Rather, a distinctly biphasic response is observed reminiscent of the Crabtree effect observed in other systems.

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