Source Paper
Nogo Receptor Antagonism Promotes Stroke Recovery by Enhancing Axonal Plasticity
Jung-Kil Lee, Ji-Eun Kim, Michael Sivula, Stephen M. Strittmatter
Journal of Neuroscience • 2004
Stroke Recovery Assessment in Mutant Mice
Objective: Examine whether blockade of the Nogo-NogoReceptor (NgR) pathway enhances axonal sprouting and recovery of complex motor function after focal brain infarction in mutant mice compared to control animals
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Materials1
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Protocol Steps
Induce focal brain infarction
Perform middle cerebral artery occlusion in mice to create stroke model
Note: Procedure performed on NgR mutant, Nogo-AB mutant, and control animals
View evidence from paper
“After a stroke, greater numbers of axons emanating from the undamaged cortex cross the midline”
Assess complex motor function recovery
Evaluate recovery of complex motor function in mutant and control animals after stroke
Note: Mutant mice lacking NgR or Nogo-AB recover more completely than control animals
View evidence from paper
“Mutant mice lacking NgR or Nogo-AB recover complex motor function after stroke more completely than do control animals”
Administer NgR blocking therapy (rat studies)
Intracerebroventricular administration of function-blocking NgR fragment in rats with middle cerebral artery occlusion
Note: Therapy initiated at subacute timepoint after stroke
View evidence from paper
“Behavioral improvement occurs when therapy is initiated 1 week after arterial occlusion”
Measure axonal plasticity
Quantify axons emanating from undamaged cortex crossing midline to innervate contralateral red nucleus and ipsilateral cervical spinal cord
Note: Axonal plasticity is enhanced in ngr-/- or nogo-ab-/- mice
View evidence from paper
“greater numbers of axons emanating from the undamaged cortex cross the midline to innervate the contralateral red nucleus and the ipsilateral cervical spinal cord; this axonal plasticity is enhanced in ngr-/- or nogo-ab-/- mice”