Motor deficit induced by red nucleus lesion: re-appraisal using kainic acid destructions.

The motor deficits induced by red nucleus lesions have been well documented but so far based upon approaches destroying both cells and fibres of passage. In the present study we used kaïnic lesions, which are known to spare, at least partially, the fibres of passage in order to re-investigate the motor deficit induced by rubral lesion. Five cats were fully trained to perform a forepaw pointing movement towards a moving spot of light. Four of them underwent a bilateral neurotoxic lesion of the red nucleus; a fifth one, was used as a control, with the lesion being done electrolytically. Kaïnic lesions induced strong dysmetria with a tendency to over-reaching, and a delayed movement onset; after postoperative training, the dysmetria only persisted when reaching towards targets moving at high speed. The electrolytic lesion led to a much stronger deficit with an additional lengthening of the execution phase duration. Moreover, although overall accuracy could recover, time taken for movement initiation and execution stayed permanently impaired. In the light of these results a distinction can be made between the red nucleus syndrome per se and the one due to damage to fibres of passage.