Effect of mercuric chloride and lead acetate treatment during the second stage of rapid post-natal brain growth on the behavioral response to chlorpromazine and on δ-ALA-D activity in weaning rats

During the early post-natal period the brain is extremely sensitive to external agents. In the present study, we examined the effects of the treatment with lead acetate (3.5 or 7.0 mg/kg) and mercuric chloride (2.5 or 5.0 mg/kg) during the early post-natal period (day 8-12) on the behavioral response to chlorpromazine (CPZ) of 22-day-old rats. The effects of these metals on the sulfhydryl-containing enzyme delta -aminolevulinate dehydratase (delta -ALA-D) were also investigated. Mercuric chloride (2.5 mg/kg) did not affect brain enzyme activity, but caused a significant stimulation of renal delta -ALA-D of 24-day-old rats (27%), while animals treated with 5 mg/kg HgCl2 showed a small but significant inhibition of cerebral (10%) and renal delta -ALA-D activitv (15%). Lead acetate (3.5 or 7 mg/kg) treatment did not affect renal or cerebral delta -ALA-D. Mercuric chloride treatment (5 mg/kg) changed the pattern of open-field activity and the CPZ-induced catalepsy. However, since the undernutrition that accompanied the metal treatment also caused changes in CPZ-induced catalepsy, the effect of mercury on catalepsy could not be clearly established. Lead acetate treatment (7 mg/kg) changed the pattern of open-field motor activity and abolished the decrease in activity observed in control rats. The cataleptic response of animals to CPZ was also affected by lead acetate treatment (7 mg/kg). The increase in activity is compatible with the hyperactivity described in animals exposed to lead for long periods. Thus, the present study suggests that a short exposure to lead or mercury during suckling (second stage of rapid post-natal brain growth) caused permanent changes in locomotor activity that can be interpreted as hyperactivity. Additionally, the behavioral response to CPZ was affected by metal treatment indicating an alteration in the dopaminergic system. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.