1. Paradoxical Motor Recovery From a First Stroke After Induction of a Second Stroke: Reopening a Postischemic Sensitive Period
- Author
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Steven R. Zeiler, Robert Hubbard, Kwan L. Ng, Tony Zheng, Ellen M. Gibson, Richard O'Brien, and John W. Krakauer
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Movement disorders ,Period (gene) ,Clinical Sciences ,Ischemia ,Inbred C57BL ,Article ,Functional Laterality ,03 medical and health sciences ,Mice ,recovery ,0302 clinical medicine ,Full recovery ,sensitive period ,Internal medicine ,medicine ,Animals ,cardiovascular diseases ,Stroke ,Movement Disorders ,Animal ,Rehabilitation ,Motor Cortex ,Stroke Rehabilitation ,Neurosciences ,General Medicine ,Recovery of Function ,medicine.disease ,stroke ,motor ,Brain Disorders ,Mice, Inbred C57BL ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Anesthesia ,Disease Models ,Cardiology ,Motor recovery ,Cognitive Sciences ,Forelimb ,medicine.symptom ,Psychology ,030217 neurology & neurosurgery ,Motor cortex - Abstract
Background and objective. Prior studies have suggested that after stroke there is a time-limited period of increased responsiveness to training as a result of heightened plasticity—a sensitive period thought to be induced by ischemia itself. Using a mouse model, we have previously shown that most training-associated recovery after a caudal forelimb area (CFA) stroke occurs in the first week and is attributable to reorganization in a medial premotor area (AGm). The existence of a stroke-induced sensitive period leads to the counterintuitive prediction that a second stroke should reopen this window and promote full recovery from the first stroke. To test this prediction, we induced a second stroke in the AGm of mice with incomplete recovery after a first stroke in CFA. Methods. Mice were trained to perform a skilled prehension (reach-to-grasp) task to an asymptotic level of performance, after which they underwent photocoagulation-induced stroke in CFA. After a 7-day poststroke delay, the mice were then retrained to asymptote. We then induced a second stroke in the AGm, and after only a 1-day delay, retrained the mice. Results. Recovery of prehension was incomplete when training was started after a 7-day poststroke delay and continued for 19 days. However, a second focal stroke in the AGm led to a dramatic response to 9 days of training, with full recovery to normal levels of performance. Conclusions. New ischemia can reopen a sensitive period of heightened responsiveness to training and mediate full recovery from a previous stroke.
- Published
- 2016