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To reveal contributions of different subdivisions of the lateral geniculate nucleus (LGN) to visuomotor behavior, segments of either layer A or the C layers were inactivated with microinjections of gamma-aminobutyric acid while cats made saccades to retinally stabilized spots of light placed either in affected regions of visual space or mirror-symmetric locations in the opposite hemifield. Inactivating layer A reduced the success rate for saccades to targets presented in affected locations from 82.4 to 26.8% while having no effect on saccades to the control hemifield. Saccades to affected sites had reduced accuracy and longer initiation latency and tended to be hypometric. In contrast, inactivating C layers did not affect performance. Data from all conditions fell along the same saccade velocity/amplitude function ("main sequence"), suggesting that LGN inactivations cause localization deficits, but do not interfere with saccade dynamics. Cerebral cortex is the only target of the A layers, so behavioral decrements caused by inactivating layer A must be related to changes in cortical activity. Inactivating layer A substantially reduces the activity of large subsets of corticotectal cells in areas 17 and 18, whereas few corticotectal cells depend on C layers for visually driven activity. The parallels between these behavioral and electrophysiological data along with the central role of the superior colliculus in saccadic eye movements suggests that the corticotectal pathway is involved in both deficits and remaining capacities resulting from blockade of layer A.

Effects of Focal Inactivation of Dorsal or Ventral Layers of the Lateral Geniculate Nucleus on Cats' Ability to See and Fixate Small Targets