Perinatal-lesion-induced Reorganization of Cerebral Functions Revealed Using Reversible Cooling Deactivation and Attentional Tasks

• Published in: Cerebral cortex (New York, N.Y. 1991) N.Y. 1991), 2001-03, Vol.11 (3), p.194-209
• Main Authors: Lomber, Stephen G., Payne, Bertram R.
• Format: Article
• Language: English
• Subjects: Acoustic Stimulation - methods; Animals; Animals, Newborn; Attention - physiology; Brain Mapping - methods; Cats; Cerebral Cortex - physiology; Female; Male; Neuronal Plasticity - physiology; Parietal Lobe - physiology; Photic Stimulation - methods; Temporal Lobe - physiology; Visual Cortex - injuries; Visual Cortex - physiology
• ISSN: 1047-3211; 1460-2199; 1460-2199
• DOI: 10.1093/cercor/11.3.194

We tested the concept that lesions of primary visual cortical areas 17 and 18 sustained on the day of birth induce a redistribution of cerebral operations underlying the ability to disengage visual attention and then redirect it to a new location. In cats, these operations are normally highly localizable to posterior middle suprasylvian (pMS) cortex. Three stimulation paradigms were used: (i) movement of a high contrast visual stimulus into the visual field; (ii) illumination of a static light-emitting diode (LED) stimulus; and (iii) a control static auditory stimulus. To test for the redistribution of critical neural operations, cryoloops were implanted bilaterally in the pMS sulcus and in contact with ventral posterior suprasylvian (vPS) cortex. Separate and combined deactivations of pMS and vPS cortices in cats with early lesions of primary visual cortex showed that full, unilateral deactivation of pMS cortex only partially impaired the ability to detect and orient to stimuli moved into the contracooled hemifield. Much more complete impairment required the additional deactivation of ipsilateral vPS cortex. Bilateral pMS deactivation alone, or in combination with bilateral vPS deactivation, largely reversed the unilateral contracooled neglect. For the orienting to static, illuminated LED stimuli, unilateral deactivation of pMS cortex was sufficient to fully impair orienting to stimuli presented in the contracooled hemifield. Bilateral pMS deactivation induced an almost complete visual-field-wide neglect of stimuli. On its own, unilateral deactivation of vPS cortex was without effect on either task, although bilateral vPS deactivations introduced inconsistencies into the performance. Termination of cooling reversed all deficits. Finally, neither the initial lesion of areas 17 and 18 nor cooling of either the MS or vPS cortex alone, or in combination, interfered with orienting to sound stimuli. Overall, our results provide evidence that at least one highly localizable visual function of normal cerebral cortex is remapped across the cortical surface following the early lesion of primary visual cortical areas 17 and 18. Moreover, the redistribution has spread the essential neural operations from the visual parietal cortex to a normally functionally distinct type of cortex in the visual temporal system.