Long-term neurochemical changes after visual cortical lesions in the adult cat

Peripheral deafferentation alters cortical function and such alterations have been shown to affect the cortical expression of the calcium-binding proteins calbindin and parvalbumin and of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). To determine whether cortical deafferentation produces similar effects, we examined the long-term consequences of cortical lesions on the neurochemistry of interconnected cortical areas. We studied the reciprocal effects of localized damage to either visual cortical areas 17 and 18, or posteromedial lateral suprasylvian (PMLS) cortex in the adult cat. These areas are strongly interconnected and play an important role in the processing of visual information. Combined lesions of areas 17 and 18 caused a marked, topographically specific decrease in the proportion of neurons expressing calbindin in supragranular layers of PMLS cortex. Similarly, lesions of PMLS cortex caused topographically restricted decreases in calbindin expression within supragranular layers of areas 17 and 18, but not in other cortical areas with which PMLS is interconnected. To categorize the calbindin-positive neurons affected by such lesions, we carried out double-labeling experiments for the inhibitory neurotransmitter GABA. This investigation showed lesions of areas 17 and 18 to affect calbindin-positive excitatory and inhibitory neurons equally, but PMLS lesions had stronger effects on inhibitory, calbindin-positive neurons. This finding may represent differential damage to feed-forward vs. feed-back projections in the two types of lesions. Finally, the expression of parvalbumin and GABA was unchanged, even in zones of decreased calbindin immunoreactivity. Our results suggest that damage to adult visual cortical areas, whether striate or extrastriate, induces neurochemical changes in the supragranular corticocortical network to which these areas belong. That changes were restricted to calbindin expression suggests cell-specific and/or biochemical pathway-specific alterations in calcium homeostasis.