Sensory processing in the cortex remains generally robust despite neuron loss due to aging, and even during the accelerated degeneration seen in prodromal phases of neurodegenerative diseases. In this study, we investigated the robustness of sound representation in the mouse auditory cortex, where sensory information is organized into population-level representational maps. Specifically, we examined how these maps are stabilized by homeostatic network mechanisms following neuronal loss. We performed longitudinal two-photon calcium imaging to track population responses to a diverse set of sound stimuli, combined with targeted microablation of functionally characterized neurons. Unilateral ablation of 30–40 highly sound-responsive neurons in layer 2/3 caused a transient disruption of the representational map, followed by recovery within 3–5 days. At the single-neuron level, this recovery was largely driven by previously unresponsive neurons that gained sound responsiveness after ablation, through enhanced correlation within the local network. In contrast, targeted ablation of inhibitory neurons led to a prolonged disruption of the representational map, primarily marked by reduced trial-to-trial reliability in sound responses. Together, these findings reveal a link between the plasticity of individual neurons and the stability of population-level representational maps, highlighting homeostatic mechanisms that preserve sensory processing in neocortical circuits.
Noda et al. (2025) studied this question.