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Activating excitatory neurons after stroke enhances functional recovery by reducing microglia-mediated synaptic pruning. This involves decreasing C1q binding to exposed phosphatidylserine (EPS) at synapses, highlighting a novel therapeutic target for stroke repair.

Keywords:
complement C1qmotor cortexneuronal plasticityphosphatidylserinesstroke

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Activating glutamatergic neurons in the motor cortex aids post-stroke functional recovery.
  • The precise molecular pathways driving this recovery are not fully understood.
  • Identifying these mechanisms is crucial for developing effective neuromodulation strategies.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which activating excitatory neurons promotes functional recovery after stroke.
  • To investigate the role of microglia-mediated synaptic pruning in this process.
  • To identify potential therapeutic targets for stroke treatment.

Main Methods:

  • Photothrombotic stroke model in mice with chemogenetic activation of excitatory neurons.
  • Evaluation of functional recovery using cylinder and grid-walking tests.
  • Analysis of microglia-mediated synaptic pruning, C1q, and exposed phosphatidylserine (EPS) levels via immunofluorescence, qPCR, Western blotting, and RNA sequencing.

Main Results:

  • Excitatory neuron activation significantly improved motor function and reduced microglia-mediated synaptic pruning.
  • Activation decreased synaptic C1q and EPS levels, while inhibition worsened outcomes.
  • Blocking EPS inhibited C1q tagging and microglia pruning, restoring synaptic density and motor function.

Conclusions:

  • Neuronal activation after stroke inhibits microglia-mediated synaptic pruning.
  • The C1q-EPS interaction at synapses is a key mechanism in post-stroke repair.
  • Targeting C1q binding to EPS offers a potential therapeutic strategy for stroke recovery.