title: Targeted mini-strokes produce changes in interhemispheric sensory signal processing that are indicative of disinhibition within minutes.
abstract: Most processing of sensation involves the cortical hemisphere opposite (contralateral) to the stimulated limb. Stroke patients can exhibit changes in the interhemispheric balance of sensory signal processing. It is unclear whether these changes are the result of poststroke rewiring and experience, or whether they could result from the immediate effect of circuit loss. We evaluated the effect of mini-strokes over short timescales (<2 h) where cortical rewiring is unlikely by monitoring sensory-evoked activity throughout much of both cortical hemispheres using voltage-sensitive dye imaging. Blockade of a single pial arteriole within the C57BL6J mouse forelimb somatosensory cortex reduced the response evoked by stimulation of the limb contralateral to the stroke. However, after stroke, the ipsilateral (uncrossed) forelimb response within the unaffected hemisphere was spared and became independent of the contralateral forelimb cortex. Within the unaffected hemisphere, mini-strokes in the opposite hemisphere significantly enhanced sensory responses produced by stimulation of either contralateral or ipsilateral pathways within 30-50 min of stroke onset. Stroke-induced enhancement of responses within the spared hemisphere was not reproduced by inhibition of either cortex or thalamus using pharmacological agents in nonischemic animals. I/LnJ acallosal mice showed similar rapid interhemispheric redistribution of sensory processing after stroke, suggesting that subcortical connections and not transcallosal projections were mediating the novel activation patterns. Thalamic inactivation before stroke prevented the bilateral rearrangement of sensory responses. These findings suggest that acute stroke, and not merely loss of activity, activates unique pathways that can rapidly redistribute function within the spared cortical hemisphere.
authors.affiliation: Department of Psychiatry and Brain Research Center, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.
authors.forename: Majid H
authors.initials: MH
authors.lastname: Mohajerani
authors.forename: Khatereh
authors.initials: K
authors.lastname: Aminoltejari
authors.forename: Timothy H
authors.initials: TH
authors.lastname: Murphy
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005552:Forelimb / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008954:Models, Biological; D009473:Neuronal Plasticity; D010841:Pia Mater / Q000378:metabolism; D013003:Somatosensory Cortex / Q000502:physiology; D020521:Stroke / Q000503:physiopathology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013788:Thalamus / Q000502:physiology; D056969:Voltage-Sensitive Dye Imaging / Q000379:methods
chemical_list: D013779:Tetrodotoxin