Visual cortical lesions in the rat and a conditioned emotional response.

Abstract

Visual decortication failed to affect rate of acquisition of 1-min. delayed CERs when either light alone or noise alone provided the CS. However, CER paradigms involving a combination of light and noise CSs revealed differences in behavior between experimental and control animals. Decorticate rats transferred the CER from light to noise (although not from noise to light). Normal animals showed no transfer. Decorticate animals were conditioned to a noise CS in a paradigm which prevents conditioning in normal subjects. Also, decorticate rats were better able to discriminate a compound light-noise CS from light-alone and noise-alone CSs. Partly from these findings, partly because the abnormal behavior of the decorticate subjects is mimicked by normal animals wearing light-diffusing eye occluders, and partly from other considerations, it was speculated that vision as a qualitatively unique sensory modality is undermined by visual cortex destruction.The nature of vision in animals lacking visual cortex appears to be in dispute. Kliiver's (1942) study, considered by some to be the classic one in the field, suggests that the visually decorticate animal is reduced largely to the use of luminous flux cues. However, work prior to Kliiver's study (e.g.,

Reversal set formation in the visually decorticate rat.

“…Also, the 50%-70% fewer errors to criterion enjoyed by normal animals in acquiring one version of a light-dark discrimination task is eliminated when both the normal and the posterior decorticate rats must learn the habit under the diffuse-light condition (Cooper, Blochert, Gillespie, & Miller, 1972). Since eliminating visuospatial task requirements removes visual-cortexrelated deficits (see also Gillespie & Cooper, 1973), the role of visual cortex seems largely to involve the perceptual processing of visuospatial information.…”

Recovery of function after brain damage: The chronic consequence of large neocortical injuries.

“…For example, drugs, in particular 8-azaguanine, which interfere with acquisition and thus prevents the new learning required by a compensatory shift, will actually facilitate recovery of function after neocortical brain injury (Davis & LeVere, 1979). The lesion-induced compensatory shift is also evident in experiments in which brain-injured animals are trained on multiple cue discriminations involving sensory cues processed by the injured neural system and sensory cues processed by noninjured neural systems (Gillespie & Cooper, 1973; LeVere & LeVere, 1982). In these investigations, it was found that the brain-injured animal invariably responded to the cues that did not involve the injured neural system; for example, auditory or haptic cues as compared to visual cues following visual decortication.…”