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Neocortex saves energy by reducing coding precision during food scarcity.

Zahid Padamsey1, Danai Katsanevaki1, Nathalie Dupuy1

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Summary

During food scarcity, the brain conserves energy by reducing synaptic activity, which impairs visual processing. Leptin hormone levels are linked to this energy-saving strategy and visual function.

Keywords:
calorie restrictionhunger and satietyin vivo ATP imagingin vivo calcium imagingin vivo electrophysiologyleptinmouse primary visual cortexorientation tuningspike rate homeostasistrial-to-trial variability

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Area of Science:

  • Neuroscience
  • Metabolic research
  • Computational neuroscience

Background:

  • Information processing in the mammalian brain is energy-intensive.
  • Mechanisms regulating brain energy use and information coding during food scarcity remain unclear.

Purpose of the Study:

  • To investigate how food scarcity affects energy consumption and information coding in the mouse visual cortex.
  • To explore the role of leptin in metabolic regulation of neural coding.

Main Methods:

  • Whole-cell recordings and two-photon imaging in layer 2/3 of the mouse visual cortex.
  • Measurement of AMPA receptor conductance, synaptic ATP use, neuronal excitability, and orientation tuning.
  • Assessment of visual discrimination performance and leptin levels.

Main Results:

  • Food restriction decreased AMPA receptor conductance, reducing synaptic ATP use by 29%.
  • Neuronal excitability was maintained via increased input resistance and depolarized resting potential.
  • Despite preserved firing rates, coding precision decreased, evidenced by broadened orientation tuning (32%) and impaired visual discrimination.
  • Reduced coding precision correlated with lower leptin levels and was reversed by leptin supplementation.

Conclusions:

  • Metabolic state dynamically regulates the energy expenditure for neural coding precision in the neocortex.
  • The brain employs an energy-saving strategy during scarcity that compromises coding precision.
  • Leptin plays a crucial role in mediating the effects of metabolic state on visual cortex function.