Hypothyroid conditions during fetal development can induce severe developmental defects such as mental retardation. Thyroid dysfunction and hypothyroid conditions induced by anti-thyroid drugs may influence neuronal development during embryogenesis. Little is known, however, about the details of the mechanisms underlying the adverse effects of thyroid dysfunction on neuronal development. In this study, we examined the gene expression levels of Bcl-2 family members and Bcl-2-associated athanogene (BAG) 3 in chick cerebellum under hypothyroid conditions using a fertilized chicken egg/chick embryo model. The hypothyroid chicks exhibited a marked reduction in BAG3 protein levels concomitant with a marked increase in mitochondrial Bak1 protein levels in cerebellum while no alteration in gene expression of Bak1 was seen. Since evidence of apoptotic cell death was observed in the cerebellum under hypothyroid conditions, these results suggest that reduction in BAG3 as well as enhancement of Bak1 protein may play an important role in the apoptosis of neuronal cells under hypothyroid conditions .