# Optimal compensation for neuron death

**Authors:** David G.T. Barrett, Sophie Denève, Christian K. Machens

bioRxiv · DOI: 10.1101/029512 · bioRxiv · 2015-01-01

## TL;DR

The brain can compensate for neuron death by balancing excitation and inhibition, preserving function until a recovery boundary is reached.

## Contribution

A novel framework showing how neural circuits optimally compensate for neuron death without synaptic plasticity.

## Key findings

- Optimal compensation explains changes in tuning curves after neuron silencing in systems like the primary visual cortex.
- Compensation relies on balanced excitation and inhibition dynamics rather than synaptic plasticity.
- A recovery boundary exists where unbalanced excitation and inhibition lead to failed signal representation and symptoms.

## Abstract

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits optimally compensate for neuron death, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that optimal compensation can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic.

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/10.1101/029512/full.md

## References

57 references — full list in the complete paper: https://tomesphere.com/paper/10.1101/029512/full.md

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Source: https://tomesphere.com/paper/10.1101/029512