Objective Nanotechnology focuses on materials having at least one dimension of less than 100 nanometers. Nanomaterials such as Nanosilver (NS) have unique physical and chemical properties such as size, shape, surface charge. NS particles are thought to in- duce neuronal degeneration and necrosis in the brain. It has been reported that NS parti- cles generate free radicals and oxidative stress which alters gene expression and induces apoptosis. This study was designed to evaluate whether the detrimental effect of NS parti- cles is through the activation of Procaspase-3 during fetal neural development. Materials and Methods In this experimental study, thirty Wistar female rats at day one of pregnancy were semi-randomly distributed into three groups of ten. Group 1, the control group, had no treatment. From day 1 to the end of pregnancy, groups 2 and 3 received 1 and 10 ppm NS respectively via drinking water. Newborn rats were sacrificed immediately after birth and their brains were dissected and kept frozen. Total RNA, extracted from brain homogenates, was reverse transcribed to cDNA. Quantitative real-time polymerase chain reaction (PCR) analysis was undertaken to estimate the expression level of Procaspase-3. Results Developmental exposure to NS induced neurotoxicity and apoptosis. This corre- lated with a significant increase in Procaspase-3 expression level especially at 10 ppm NS. Conclusion The pro-apoptotic activity of NS in cells is likely to due to the dysregula- tion of Procaspase-3.