Literature DB >> 3251605

Sparing of skilled forelimb reaching and corticospinal projections after neonatal motor cortex removal or hemidecortication in the rat: support for the Kennard doctrine.

I Q Whishaw1, B Kolb.   

Abstract

Skilled forelimb use in reaching for food was studied in rats with variously sized and placed unilateral cortical lesions given in adulthood or on the day of birth. Fluorescent retrograde labelling was used to document changes in corticospinal tracts. In free choice tests, preferential use of the limb ipsilateral to damage was induced by adult motor, but not parietal or occipital, cortex damage. Similar preference for the ipsilateral limb was induced by neonatal motor and parietal, but not occipital, cortex damage. In both adult and neonate groups success with the preferred limb decreased in proportion to the increase in lesion size. To force use of the non-preferred limb, a bracelet, which prevented reaching but not other movements, was attached to the forearm of the preferred forelimb. Success with the non-preferred limb was poorer than with the preferred limb and success again decreased in proportion to the increase in lesion size. Adult and neonatal rats were divided into 4 groups according to the extent of motor cortex damage. Across all lesion sizes the neonatal operates were significantly more successful than the adult operates and their reaching movements appeared more normal. Surprisingly, some rats with large adult motor cortex lesions or hemidecortications were able to reach. Slow-motion video analysis of reaching impairments in both adult and neonate groups showed that limb extension and food grasping were less impaired than limb retraction and adduction of the limb to the mouth. The results show that the integrity of a neocortical hemisphere is not essential for contralateral limb use in reaching, but contributes to successful use of the limb. Following neonatal lesions, facilitation may be promoted by the ipsilateral neocortex through an augmented ipsilateral corticofugal pathway.

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Year:  1988        PMID: 3251605     DOI: 10.1016/0006-8993(88)90753-6

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


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