Abstract
The effects of triethyl lead acetate (triethyl Pb) on the cholinergic system in the brain of the rats were investigated in vitro. Triethyl Pb, at concentrations below 10-4 M, inhibited the depolarized release of acetylcholine (ACh) from slices of cortex and they synthesis of ACh in such slices, while it potentiated in a dose-dependent manner the non-depolarized release of ACh. In contrast, lead inhibited noncompetitively the high-affinity uptake of choline into synaptosomes with a Ki of 4.03 × 10-6 M and the activity of choline acetyltransferase with a Ki of 4.07 × 10-5 M. Triethyl Pb has an inhibitory effect (IC50 ≈ 5 × 10-5 M) on the binding of [3H]quinuclidinyl benzilate to muscarinic ACh receptors. Triethyl Pb inhibited acetylcholinesterase activity slightly at 5 × 10-5 and 10-4 M. It is suggested that ACh transmission, in particular the synthesis of ACh and the release of ACh, is susceptible to organolead neurotoxicity.
