Abstract

We have studied the visually triggered orienting behavior of frogs following complete unilateral transection of the neuraxis at the junction of the medulla and spinal cord, as well as after smaller lesions at the same level. Complete transection produces the same behavioral deficit as previously reported (Kostyk and Grobstein 1982, 1987a) for a similar lesion at the junction between midbrain and medulla. Lesioned frogs failed to turn toward stimuli at all locations in the ipsilateral visual hemifield, responding instead with forwardly directed movements in which there was a persistance of variations related to stimulus elevation and distance. Responses to stimuli in the contralateral visual hemifield were normal. Similar deficits were seen after smaller lesions restricted to a medial white tract. Partial damage to the tract resulted in turns of reduced amplitude for stimuli throughout the ipsilateral hemifield. Lesions to adjacent tissue were without effect on the behaviors studied. In all animals, we observed a strong correlation between turn amplitude for lateral stimuli and the distance at which the animals switched from snapping to hopping. These observations provide new evidence that a transformation from a retinocentric to a lateralized and parcellated form of spatial representation occurs in going from the retinotectal projection to the descending tectofugal pathway in the caudal midbrain, and that this form of representation remains stable until the spinal cord. A second transformation involved in determining the actual movement to be triggered must occur subsequently. Our findings also suggest that the signals underlying orienting turns may not descend into the spinal cord on tectospinal axons, and suggest that the lateralization of descending signals probably occurs coincidentally with a synaptic relay in the midbrain tegmentum.

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