ALTERATIONS IN CENTRAL MONOAMINE SYSTEMS AFTER POSTNATAL LEAD ACETATETREATMENT IN RATS

The present study was undertaken to investigate the effects of postnat al lead exposure on central monoamine systems. Newborn male Sprague-Da wley rats were given 1 or 8 mg/kg lead acetate intraperitoneally for 2 0 days postnatally. Two groups of control rats received sodium acetate , or sodium acetate in oversized litters to compensate for lead-induce d malnutrition in the high lead dose group, while nontreated animals a lso served as controls. At Day 21 or 51 regional tissue levels of mono amines were determined using HPLC techniques. No major changes were se en after the lead exposures in the levels of dopamine, noradrenaline, and serotonin, or metabolites of dopamine and serotonin, when compared to respective control groups. On the other hand, in the control group given sodium acetate in oversized litters some alterations of the mon oamine levels were observed in frontal cortex and striatum at Day 21 c ompared to controls. At Day 51, the striatal homovanillic acid and 5-h ydroxyindoleacetic acid levels were higher in the low lead dose group compared to those in the controls. No other changes in the monoamine l evels were seen at Day 51. At 50-70 days postnatally, potassium-stimul ated dopamine overflow was studied in striatum with in vivo chronoampe rometry. In the high lead dose group the amplitudes of signals were lo wer in both the dorsal and ventral striatum compared to the controls, while no difference was seen in the clearance time of dopamine. The ca pacity of the dopamine terminals to respond to repeated stimulation wa s not affected by the lead exposure. Thus, the steady-state levels of monoamines were essentially unaltered after postnatal lead exposure in rats, while functional aspects of striatal dopamine transmission were affected after exposure to the higher dose of lead. These findings su pport the hypothesis that lead-induced changes in motor skills and exp loratory behavior may be related to altered dopamine neurotransmission . (C) 1994 Academic Press, Inc.