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Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis
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CREB controls cortical circuit plasticity and functional recovery after stroke
L Caracciolo1, M Marosi1,2, J Mazzitelli1
1Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Nature Communications
|June 10, 2018
Summary
Enhancing neuronal excitability via cAMP-response-element binding protein (CREB) boosts motor recovery post-stroke. Manipulating CREB activity in motor neurons can control the restoration of motor function after brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Neurorehabilitation
Background:
- Neuronal excitability is crucial for motor function recovery after stroke.
- cAMP-response-element binding protein (CREB) is a key transcription factor regulating neuronal excitability.
Purpose of the Study:
- To investigate the role of CREB in motor recovery after stroke.
- To determine if manipulating CREB activity can modulate stroke recovery.
Main Methods:
- Utilized viral vectors to increase CREB levels in motor neurons.
- Employed hM4Di-DREADD to silence CREB-transfected neurons in the peri-infarct region.
- Assessed motor performance and circuit remapping post-stroke.
Main Results:
- Increased CREB levels enhanced motor recovery after stroke.
- Blocking CREB signaling prevented stroke recovery, which was reversible upon disinhibition.
- CREB transfection promoted remapping and new connection formation in motor and somatosensory circuits.
Conclusions:
- CREB is a central regulator of neuronal circuit responses driving motor recovery post-stroke.
- Targeting CREB activity offers a potential therapeutic strategy to control stroke recovery outcomes.
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