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Slice Patch Clamp Technique for Analyzing Learning-Induced Plasticity
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Paradoxical lesions, plasticity and active inference.

Noor Sajid1, Thomas Parr1, Andrea Gajardo-Vidal1

  • 1Wellcome Centre for Human Neuroimaging, University College London, London WC1N 3AR, UK.

Brain Communications
|December 30, 2020
PubMed
Summary
This summary is machine-generated.

Secondary brain lesions can surprisingly improve function. Our study simulated how altering the balance of excitation and inhibition in the brain can reverse deficits, offering new insights into recovery after injury.

Keywords:
active inferencelearningparadoxical lesionsplasticitystructure–function relationship

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Area of Science:

  • Neuroscience
  • Computational Biology
  • Systems Neuroscience

Background:

  • Paradoxical lesions are secondary brain injuries that improve functional deficits from an initial insult.
  • Existing theories involve reduced inhibition or increased excitatory-to-inhibitory balance in surrounding tissue.
  • Understanding the mechanisms of paradoxical lesions is crucial for predicting recovery after brain injury.

Purpose of the Study:

  • To simulate how and when changes in the excitatory-inhibitory balance trigger functional deficit reversal after a primary lesion.
  • To investigate the role of intrinsic and extrinsic connectivity in paradoxical lesion effects.
  • To predict the physiological correlates of paradoxical lesions using a computational model.

Main Methods:

  • Introduction of in-silico lesions into an active inference model of auditory word repetition.
  • Simulation of damage to extrinsic connectivity (primary lesion) and intrinsic connectivity (secondary lesion).
  • Analysis of experience-dependent plasticity and its effect on performance with varying lesion severity.

Main Results:

  • A mild secondary lesion to intrinsic connectivity enhanced performance through increased plasticity, demonstrating a paradoxical lesion effect.
  • The paradoxical effect disappeared with a severe secondary lesion due to amplified plasticity in intrinsic connectivity.
  • The computational framework predicted physiological correlates of paradoxical lesions.

Conclusions:

  • Modifications in the excitatory-inhibitory balance, particularly within intrinsic connectivity, can drive functional recovery after brain lesions.
  • The severity of secondary lesions critically influences the manifestation of the paradoxical lesion effect.
  • This computational approach offers novel insights into the neurophysiological mechanisms underlying recovery from brain damage.