Komulainen H, Pietarinen R, Tuomisto J
Acta Pharmacol Toxicol (Copenh). 1983 May;52(5):381-9. doi: 10.1111/j.1600-0773.1983.tb01118.x.
Adult male Wistar rats were administered acute toxic doses of lead (Pb), triethyl lead (TriEL) or tetraethyl lead (TEL) by gavage. The ability of striatal, hypothalamic and cortical synaptosomes to take up tritiated monoamines was assayed 24 hours later. Pb, TriEL as well as TEL increased dopamine (DA) uptake into striatal synaptosomes at least at some dose level. Pb increased, but TEL decreased 5-hydroxytryptamine(5-HT) uptake into hypothalamic synaptosomes, while TEL increased noradrenaline (NA) uptake into cortical synaptosomes. After a 3 week administration to initially 4 week old rats of even toxic doses of Pb in drinking water, monoamine uptake was not significantly affected. On the contrary, the neurotoxicity of TEL was cumulative in that a much lower dose decreased 5-HT uptake when divided over a 3 week period than acutely. In vitro TriEL inhibited DA uptake (IC50; 0.8 microM) into striatal and 5-HT uptake (5.0 microM) into hypothalamic synaptosomes but TEL and delta-aminolevulinic acid did not. The results suggest that dopaminergic and serotonergic neurones differ in their response to alkyl lead in vivo. The differences could be due to basic differences in the neurochemical behaviour of these two types of nerve endings.