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Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery
Published on: July 31, 2014
Middle cerebral artery (MCA) stroke produces dysfunction in adjacent motor cortex as detected by intracortical
O A Gharbawie1, C L R Gonzalez, P T Williams
1Department of Psychology and Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta, Canada T1K 3M4. omar.gharbawie@uleth.ca
Abstract:
Middle cerebral artery (MCA) stroke in the rat produces impairments in skilled movements. The lesion damages lateral neocortex but spares primary motor cortex (M1), raising the question of the origin of skilled movement deficits. Here, the behavioral deficits of MCA stroke were identified and then M1 was examined neurophysiologically and neuroanatomically. Rats were trained on a food skilled reaching task then the lateral frontal cortex was damaged by unilateral MCA electrocoagulation contralateral to the reaching forelimb. Reach testing and training on two tasks was conducted over 30 post-surgical days. Later, M1 and the corticospinal tract were investigated using intracortical microstimulation (ICMS), anterograde and retrograde axon tracing. A skilled reaching impairment was observed post-surgery, which partly recovered with time and training. ICMS revealed a diminished forelimb movement representation in MCA rats, but a face representation comparable in size to sham rats. Anterograde and retrograde tract tracing suggest that M1 efferents were intact. Although M1 appears to be in the main anatomically spared after MCA stroke its function as assessed electrophysiologically and behaviorally is disrupted.
Insights
Middle cerebral artery (MCA) stroke impairs skilled movements by affecting brain function, not just structure. This study reveals disrupted primary motor cortex (M1) function after MCA stroke, despite anatomical sparing.
Area of Science:
- Neuroscience
- Motor Control
- Stroke Research
Background:
- Middle cerebral artery (MCA) stroke in rats causes skilled movement deficits.
- The lesion impacts lateral neocortex, sparing primary motor cortex (M1), creating a need to understand deficit origins.
Purpose of the Study:
- To identify behavioral deficits after MCA stroke.
- To investigate the neurophysiological and neuroanatomical state of M1 post-MCA stroke.
Main Methods:
- Rats underwent MCA electrocoagulation, followed by skilled reaching tasks over 30 days.
- Primary motor cortex (M1) and corticospinal tract were examined using intracortical microstimulation (ICMS) and axon tracing.
Main Results:
- MCA stroke induced skilled reaching impairments, with partial recovery through training.
- ICMS showed a reduced forelimb representation but normal face representation in M1.
- Axon tracing indicated intact M1 efferents.
Conclusions:
- MCA stroke disrupts M1 function, evidenced by behavioral and electrophysiological changes.
- Despite anatomical sparing, M1's role in skilled movement is compromised post-stroke.
