Apoptosis, a programmed, non-inflammatory type of cell death, is a key homeostatic mechanism in all organisms. In the nervous system of rodents, pronounced apoptotic neuronal loss takes place during the first days of life, and early neuronal activity is one of the essential factors regulating this process.The project aimed to investigate the effects of local neuronal silencing on postnatal apoptosis and cortical activity. New-born mice were implanted with drug-loaded polymers to achieve local and chronic neuronal inactivation in the somatosensory cortex. Subsequent combination of in vivo electrophysiology, wide field calcium imaging and immunohistochemistry, allowed us to characterize both postnatal pan-cortical activity dynamics and cell death.Our results confirmed a fast and successful silencing, effective shortly after start of the treatment. Chronic inactivation in mouse pups at P4 exacerbated developmental cell death and resulted in a peak of cortical apoptosis after 24h, which extended though the entire cortical depth and beyond the target region. Thus, effects on cell death levels were also investigated in directly and indirectly connected areas, such as caudatoputamen and hippocampus. Finally, wide field calcium imaging recordings allowed us to assess the effect of local silencing on activity levels in neighbouring and distant cortical regions.Taken together, the results of this direct in vivo approach confirm that local cortical silencing of neuronal activity increases cell death, and suggest that direct and indirect effects of local changes in activity in the developing brain should be carefully considered.Funded by CRC1080 (project A01).