Effects of chronic lead exposure on release of endogenous catecholamines: a preliminary communication.
The release of endogenous dopamine and norepinephrine from six brain regions (cortex, hippocampus, hypothalamus, striatum, s. nigra, n. accumbens-o. tubercle) of chronically lead-exposed rats was compared to release from controls. Prenatal and postnatal chronic lead intoxication was induced by 1000 ppm lead acetate in the drinking water of dams 70 days prior to mating and throughout gestation and lactation. Offspring were also maintained on 1000 ppm lead acetate until sacrificed at approximately 60 days of age. Release was measured in vitro from tissue minces prepared from both lead-exposed and control rats. There were no significant differences in spontaneous or potassium-stimulated norepinephrine release between lead-exposed and control rats. Potassium and amphetamine both stimulated striatal dopamine release; however, no marked differences between lead-exposed and control tissue were seen. Potassium-stimulated release of dopamine from the nucleus accumbens-olfactory tubercle area was increased in the lead-exposed animals. This is interesting in light of the postulated role of the n. accumbens in the central regulation of motor activity and the reported alterations in activity in lead-exposed rodents.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D005260:Female; D007854:Lead / Q000633:toxicity*; D008297:Male; D008431:Maternal-Fetal Exchange; D009638:Norepinephrine / Q000378:metabolism; D009942:Organometallic Compounds; D011247:Pregnancy; D051381:Rats
D002395:Catecholamines; D009942:Organometallic Compounds; D007854:Lead; C008261:lead acetate; D004298:Dopamine; D009638:Norepinephrine