Behavioral and neurophysiological effects of delayed training following a small ischemic infarct in primary motor cortex of squirrel monkeys

• Published in: Experimental brain research Vol. 169; no. 2; p. 106
• Main Authors: Barbay, S, Plautz, E J, Friel, K M, Frost, S B, Dancause, N, Stowe, A M, Nudo, R J
• Format: Journal Article
• Language: English
• Published: Heidelberg Springer Nature B.V 01-02-2006
• ISSN: 0014-4819; 1432-1106

A focal injury within the cerebral cortex results in functional reorganization within the spared cortex through time-dependent metabolic and physiological reactions. Physiological changes are also associated with specific post-injury behavioral experiences. Knowing how these factors interact can be beneficial in planning rehabilitative intervention after a stroke. The purpose of this study was to assess the functional impact of delaying the rehabilitative behavioral experience upon movement representations within the primary motor cortex (M1) in an established nonhuman primate, ischemic infarct model. Five adult squirrel monkeys were trained on a motor-skill task prior to and 1 month after an experimental ischemic infarct was induced in M1. Movement representations of the hand were derived within M1 using standard electrophysiological procedures prior to the infarct and again one and two months after the infarct. The results of this study show that even though recovery of motor skills was similar to that of a previous study in squirrel monkeys after early training, unlike early training, delayed training did not result in maintenance of the spared hand representation within the M1 peri-infarct hand area. Instead, delaying training resulted in a large decrease in spared hand representation during the spontaneous recovery period that persisted following the delayed training. In addition, delayed training resulted in an increase of simultaneously evoked movements that are typically independent. These results indicate that post-injury behavioral experience, such as motor skill training, may modulate peri-infarct cortical plasticity in different ways in the acute versus chronic stages following stroke.