Objective To realize the potentially developmental neurotoxicity of chlorpromazine ( CPZ ) on zebrafish embryos and Larvae． Methods The effect of the general toxicity in zebrafish embryos and larvae were assessed after high doses of CPZ ( ≥5 mg /L) administered to zebrafish embryos on 6 － 72 hours post fertilization ( hpf) ． Then，pathology change and cell apoptosis were investigated． Under teratogenic dosage of CPZ ( ≤2. 0 mg /L) administered to zebrafish embryos on 6 － 72 hpf，the escape times of 3 dpf larvae in the touched -evoke escape reaction was recorded．Moreover，spontaneous movement and light-evoked startle escape response of 6 dpf zebrafish were tracked and analyzed by using a video-tracking system． Results The lethal and teratogenic effects of CPZ was dose-dependent and stagedependent． Histopathological examination revealed that brain volume and brain cells of 7 dpf larvae have reduced in size．The number of apoptotic cells of 36 hpf embryos has increased in midbrain，hindbrain，hypothalamus，midbrain hindbrain boundary，notochord as well as tail． The weaker tactile sensitivity was displayed when 3 dpf larvae were exposured to CPZ ( ≥0. 125 mg /L) ． Hypoactivity was discovered when 6 dpf larvae were exposured to CPZ ( ≥0. 5 mg /L) ． Furthermore，CPZ also evokes tremor，freezing or stereotypic circling swimming in 6 dpf larvae． CPZ ( 1. 0 mg /L or 2. 0 mg /L) can inhibit but CPZ ( 0. 125 mg /L or 0. 25 mg /L) can promote hyperactivity by light-evoked startle reaction． Conclusion CPZ can cause developmental neurotoxicity on zebrafish embryos and larvae． In addition，zebrafish larvae have obvious advantages to make it a powerful alternative for the developmental neurotoxicity assessment of exogenous compounds by using high-throughput behavioral test methods．