Objective:　To　explore　the　effects　of　lead　exposure　during　intrauterine　and　lactation　in　filial　rats　on　neuron　apoptosis　and　the　expressions　of　bcl-2　and　bax　genes　in　hippocampus　formation　and　the　relationship　between　them.　Methods:　SD　rats　were　exposed　to　2000　mg·L-1　of　lead　acetate　in　their　drinking　water　for　6　weeks,　and　then　mated.　Their　offsprings　were　exposed　to　lead　only　during　intrauterine　and　lactation.　At　postnatal　day　21　(PN21d),　the　neuron　apoptosis　was　examined　with　terminal　deoxynucleotidyl　transferase　mediated　dUTP　biotined　nicked　end　labeling　(TUNEL)　in　the　different　hippocampal　subareas.　The　expressions　of　the　bcl-2　and　bax　gene　were　examined　with　SP　immuno-histochemistry.　Results:　The　indices　of　neuron　apoptosis　in　CA1,　CA3　and　DG　regions　of　lead-exposed　offsprings　were　significantly　higher　than　those　of　control　(P＜0.01).　The　expression　of　bcl-2　of　lead-exposed　offsprings　was　significantly　lower　than　those　of　control,　and　the　expression　of　bax　of　the　lead-exposed　was　significantly　higher　than　that　of　control.　Conclusions:　Lead　may　cause　neuron　apoptosis　in　the　hippocampus　through　the　down　regulation　of　bcl-2　gene　expression　and　the　up　regulation　of　bax　expression.