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

Elife. 2017 Aug 21:6:e27696. doi: 10.7554/eLife.27696.

Abstract

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.

Keywords: activity patterns; apoptosis; cell death; cerebral cortex; development; developmental biology; mouse; neuroscience; stem cells; whisker deafferentation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / physiology
  • Anesthesia
  • Animals
  • Animals, Newborn
  • Apoptosis*
  • Caspase 3 / metabolism
  • Cell Count
  • Cerebral Cortex / cytology*
  • Cerebral Cortex / embryology
  • Cerebral Cortex / physiology*
  • Electrophysiological Phenomena*
  • Mice
  • Motor Cortex / physiology
  • Neurons / cytology*
  • Neurons / metabolism
  • Somatosensory Cortex / physiology

Substances

  • Caspase 3

Grants and funding

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.