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Subnetwork-Specific Homeostatic Plasticity in Mouse Visual Cortex In Vivo.

Samuel J Barnes1, Rosanna P Sammons1, R Irene Jacobsen1

  • 1MRC Centre for Developmental Neurobiology, King's College London, New Hunt's House 4(th) Floor, London SE1 1UL, UK; Department of Neuroscience, Physiology, and Pharmacology, University College London, 21 University Street, London WC1E 6DE, UK.

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Summary

Homeostatic regulation restores some, but not all, cortical activity after sensory deprivation. A specific subnetwork of excitatory neurons recovers, while inhibitory neurons do not, suggesting targeted network mechanisms.

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Area of Science:

  • Neuroscience
  • Cortical plasticity
  • Sensory deprivation

Background:

  • Homeostatic regulation aims to restore cortical activity after sensory deprivation.
  • Previous studies indicate recovery, but the uniformity across neuronal populations remains unclear.

Purpose of the Study:

  • To investigate whether homeostatic recovery of cortical activity is uniform across all neurons or specific to a neuronal subset.
  • To examine the roles of excitatory and inhibitory neurons in cortical plasticity following sensory deprivation.

Main Methods:

  • Chronic calcium imaging in behaving adult mice.
  • Analysis of individual excitatory and inhibitory neuron activity in the visual cortex.
  • Enucleation was used to induce monocular sensory deprivation.

Main Results:

  • Only a fraction of excitatory neurons exhibited homeostatic recovery of activity post-deprivation.
  • Inhibitory neurons showed no significant recovery of activity.
  • Recovering excitatory neurons displayed correlated activity, forming a distinct subnetwork.
  • Synaptic inhibition onto excitatory neurons was reduced overall.

Conclusions:

  • Homeostatic recovery of cortical activity is not uniform and involves specific neuronal subnetworks.
  • Both synaptic mechanisms (reduced inhibition) and subnetwork dynamics contribute to cortical plasticity.
  • Excitatory-inhibitory balance plays a critical role in adapting neural circuits to sensory loss.