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Related Experiment Video

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Complement peptide C3a stimulates neural plasticity after experimental brain ischaemia.

Anna Stokowska1, Alison L Atkins1, Javier Morán1

  • 1Center for Brain Repair and Rehabilitation, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.

Brain : a Journal of Neurology
|December 14, 2016
PubMed
Summary

Complement peptide C3a enhances brain plasticity and motor function recovery after ischemic stroke. Intranasal C3a treatment promotes neural repair and synaptic density, offering a promising therapeutic strategy for stroke survivors.

Keywords:
complementintranasal treatmentmicerecoverystroke

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Area of Science:

  • Neuroscience
  • Immunology
  • Regenerative Medicine

Background:

  • Ischemic stroke causes significant long-term disability despite endogenous repair mechanisms.
  • There is a critical need for therapies to enhance brain plasticity and functional recovery post-stroke.
  • Previous research indicated complement-derived peptide C3a influences neural progenitor cell behavior and neurogenesis.

Purpose of the Study:

  • To investigate the role of C3a-C3a receptor signaling in neural plasticity following ischemic stroke.
  • To evaluate the therapeutic potential of C3a for promoting recovery in the subacute to chronic stroke phases.

Main Methods:

  • Utilized C3a receptor-deficient and C3a-overexpressing (GFAP-C3a transgenic) mice subjected to photothrombotic stroke.
  • Assessed post-stroke expression of GAP43, a marker of axonal plasticity, in the peri-infarct cortex.
  • Administered daily intranasal C3a treatment to wild-type mice starting 7 days post-stroke and evaluated motor function recovery.

Main Results:

  • C3a overexpression increased GAP43 expression, while C3a receptor deficiency decreased it, indicating C3a's role in plasticity.
  • Intranasal C3a treatment significantly enhanced synaptic density and GAP43 expression in the peri-infarct cortex.
  • C3a treatment accelerated and improved forepaw motor function recovery in mice post-stroke.

Conclusions:

  • C3a-C3a receptor signaling is a key stimulator of post-ischemic neural plasticity.
  • Intranasal administration of C3a receptor agonists represents a promising therapeutic strategy to enhance functional recovery after ischemic brain injury.