6533b832fe1ef96bd129adec

RESEARCH PRODUCT

Electrical activity controls area-specific expression of neuronal apoptosis in the mouse developing cerebral cortex

Werner KilbOriane BlanquieSalim SharopovJenq-wei YangHeiko J. LuhmannAnne Sinning

subject

0301 basic medicineAgingMouseStimulationCell CountSomatosensory systemMice0302 clinical medicineAnesthesiaBiology (General)whisker deafferentationCerebral CortexNeuronsNeocortexCaspase 3General NeuroscienceQRapoptosisMotor CortexGeneral MedicineAnatomyactivity patternsmedicine.anatomical_structurecell deathCerebral cortexMedicinePrimary motor cortexMotor cortexResearch ArticleProgrammed cell deathQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsSensory deprivationdevelopmentGeneral Immunology and MicrobiologySomatosensory CortexElectrophysiological Phenomena030104 developmental biologyDevelopmental Biology and Stem Cellsnervous systemAnimals NewbornNeuroscience030217 neurology & neurosurgeryNeuroscience

description

Programmed cell death widely but heterogeneously affects the developing brain, causing the loss of up to 50% of neurons in rodents. However, whether this heterogeneity originates from neuronal identity and/or network-dependent processes is unknown. Here, we report that the primary motor cortex (M1) and primary somatosensory cortex (S1), two adjacent but functionally distinct areas, display striking differences in density of apoptotic neurons during the early postnatal period. These differences in rate of apoptosis negatively correlate with region-dependent levels of activity. Disrupting this activity either pharmacologically or by electrical stimulation alters the spatial pattern of apoptosis and sensory deprivation leads to exacerbated amounts of apoptotic neurons in the corresponding functional area of the neocortex. Thus, our data demonstrate that spontaneous and periphery-driven activity patterns are important for the structural and functional maturation of the neocortex by refining the final number of cortical neurons in a region-dependent manner.

10.7554/elife.27696http://europepmc.org/articles/PMC5582867