Middle Cerebral Artery Occlusion
Objective: To investigate the impact of BDNF Val66Met polymorphism on motor recovery following transient middle cerebral artery occlusion-induced ischemic stroke in mice
This is a Middle Cerebral Artery Occlusion protocol using mouse as the model organism. The procedure involves 4 procedural steps. Extracted from a 2014 paper published in Journal of Neuroscience.
Model and subjects
mouse • BDNF +/+ and BDNF M/M littermates • male • Not specified • Not specified
Study window
Estimated timing pending
Core workflow
Surgical procedure - Transient middle cerebral artery occlusion • Motor function assessment • Anatomical analyses
Primary readouts
- Motor/kinematic performance
- Ipsilesional hindlimb function
- Striatum volume
- Dendritic arbor measurements
Key equipment and reagents
Verified items
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Direct vendor links
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Protocol Steps
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Surgical procedure - Transient middle cerebral artery occlusion
Male BDNF +/+ and BDNF M/M littermates received either sham surgery or transient middle cerebral artery occlusion
Note: The text does not provide detailed surgical methodology, anesthesia protocols, or specific occlusion duration
View evidence from paper
“Male BDNF +/+ and BDNF M/M littermates received sham or transient middle cerebral artery occlusion”
Motor function assessment
Motor function was assessed regularly for 6 months after stroke
Note: Specific behavioral tests and assessment methods are not detailed in the provided text
View evidence from paper
“We assessed motor function regularly for 6 months after stroke and then performed anatomical analyses”
Anatomical analyses
Anatomical analyses were performed after the 6-month motor function assessment period
Note: Specific anatomical methods are not detailed in the provided text
View evidence from paper
“We assessed motor function regularly for 6 months after stroke and then performed anatomical analyses”
Transient inactivation of contralateral striatum
Transient inactivation of the contralateral striatum was performed during recovery to test its role in enhanced motor function
Note: Specific methodology for inactivation is not detailed in the provided text
View evidence from paper
“Transient inactivation of the contralateral striatum during recovery transiently abolished the enhanced function”