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Individual components of activity and habituation of activity were determined throughout the 1st month of life in the rat pup. Total activity increased from 25% at 8 days of age to 68% at 22 days before declining to 49% at 26 days. Total slight activity (predominantly sniffing) increased to a maximum of 33% at 15 days whereas total very active behavior (predominantly ambulation) reached its maximum of 38% at 22 days. Habituation of activity expressed as the mean slope of decrement of activity over the 1st 30 min of the observation period was observed in rats as young as 8 days of age. By 12 days, habituation of total activity had increased significantly reflecting a 3-fold increase ihabituation of slight activity, an effect observed at 15 days as well. However, by 19 days the slope of activity decrement had declined to half of its 15-day value, indicating an impairment of habituation and reflecting the attenuation of very active behavior, predominantly ambulation. This decline in habituation continued through 22 days but by 26 days habituation of activity had increased again reaching a maximum for the 1st month of postnatal life. Our results suggest that the phenomenon of behavioral arousal observed in the developing rat pup 19 days of age reflects an inability of the organism to modulate his activity as effectively as the 15-day- or 26-day-old animal.

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.

Previous data in bone organ culture have demonstrated a mobile compartment of Pb regulated like bone mineral. To test for its existence in vivo,after 7mglkg of Pb plus 25vCi '03pb were given IV, TPTX rats were placed in metabolism cages; and 4 days later, EDTA or PTH was infused via a catheterized tail vein for 6 hours. Measurements were made of stable Pb and 2 0 3~b from aliquots of total organs, urinary Pblcreatinine (Pb-U) , and blood Pb (Pb-B) , pg/dl. 3 days later the rats were sacrificed and the cpm of 2 0 3~b from bone (B),liver (L),and kidney (K) were expressed as the X change vs saline-infused controls. The results (*p < .01;**