title: Alterations in central monoamine systems after postnatal lead acetate treatment in rats.
abstract: The present study was undertaken to investigate the effects of postnatal lead exposure on central monoamine systems. Newborn male Sprague-Dawley rats were given 1 or 8 mg/kg lead acetate intraperitoneally for 20 days postnatally. Two groups of control rats received sodium acetate, or sodium acetate in oversized litters to compensate for lead-induced malnutrition in the high lead dose group, while nontreated animals also served as controls. At Day 21 or 51 regional tissue levels of monoamines were determined using HPLC techniques. No major changes were seen 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 over-sized litters some alterations of the monoamine levels were observed in frontal cortex and striatum at Day 21 compared to controls. At Day 51, the striatal homovanillic acid and 5-hydroxyindoleacetic acid levels were higher in the low lead dose group compared to those in the controls. No other changes in the monoamine levels were seen at Day 51. At 50-70 days postnatally, potassium-stimulated dopamine overflow was studied in striatum with in vivo chronoamperometry. In the high lead dose group the amplitudes of signals were lower in both the dorsal and ventral striatum compared to the controls, while no difference was seen in the clearance time of dopamine. The capacity of the dopamine terminals to respond to repeated stimulation was 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 support the hypothesis that lead-induced changes in motor skills and exploratory behavior may be related to altered dopamine neurotransmission.
authors.affiliation: Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Luthman
authors.forename: E
authors.initials: E
authors.lastname: Lindqvist
authors.forename: G A
authors.initials: GA
authors.lastname: Gerhardt
authors.forename: L
authors.initials: L
authors.lastname: Olson
authors.forename: B H
authors.initials: BH
authors.lastname: Hoffer
mesh_terms: D000293:Adolescent; D000818:Animals; D000831:Animals, Newborn; D015306:Biogenic Monoamines / Q000378:metabolism*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D001923:Brain Chemistry; D004298:Dopamine / Q000378:metabolism; D004563:Electrochemistry; D006801:Humans; D008297:Male; D009942:Organometallic Compounds / Q000008:administration & dosage / Q000032:analysis / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D015306:Biogenic Monoamines; D009942:Organometallic Compounds; C008261:lead acetate; D004298:Dopamine