The neocortex generates large-scale spatiotemporal patterns of spontaneous activity that collapse when oxygen supply fails. How neurons in different cortical layers contribute to this breakdown and to subsequent recovery upon reoxygenation remains poorly understood. Using high-density silicon probe recordings spanning the depth of the rat primary somatosensory cortex, together with direct-current recordings and intracellular measurements from identified pyramidal neurons during transient oxygen deprivation, we found that spiking activity across layers rapidly declined due to progressive synaptic silencing and membrane hyperpolarization. This global quiescence was followed by a massive anoxic depolarization that consistently originated from layer 5 pyramidal neurons before propagating through the cortical column. Upon reoxygenation, neurons repolarized in a corresponding sequence and exhibited a transient rebound of synchronous firing, followed by a gradual return to baseline levels of activity within 40 min. Despite this recovery at the population level, most individual neurons showed persistent alterations in firing rates, indicating that cortical resilience to anoxia involves a redistribution of single-cell activity across layers. These findings define the laminar sequence of neuronal failure and recovery during transient cerebral anoxia and reveal layer-specific vulnerabilities that may inform strategies to preserve or restore cortical function after anoxic or ischemic injury.
Grou-Radenez et al. (Fri,) studied this question.