Lead neurotoxicity has caused wide public concern in recent decades, yet little is known about its effects on cellular and molecular mechanisms during the sensitive early life stages of animals. This study examines neurological deficits caused by lead acetate (Pb) during early embryonic stages in the zebrafish (Danio rerio) and further explores its potential molecular mechanism. Zebrafish embryos showed varying levels of toxicity, which was proportional to the concentration of Pb to which the embryos were exposed. Following Pb exposure (0.2 mM), embryos showed obvious neurotoxic symptoms with "sluggish" action, slow swimming movements and slow escape action. Whole mount in situ hybridization showed that gfap and huC gene expression patterns decreased significantly throughout the brains of the Pb-treated embryos, particularly in the diencephalon region. RT-PCR further proved the downregultion of the two genes. However, ngn1 and crestin gene expression patterns were similar in both the Pb-treated embryos and the control embryos. The TUNEL assay demonstrated that the reduction of nerve cells was due to increased apoptosis of neuron and glia cells. In conclusion, these findings identify that Pb-induced neurotoxicity can be caused by impaired neurogenesis, resulting in markedly increased apoptosis of special types of neural cells, neuron and glia cells. (C) 2011 Elsevier B.V. All rights reserved.