Influence of saccadic eye movements on geniculostriate excitability in normal monkeys

Summary Using permanently implanted electrodes in squirrel monkeys and macaques, transmission through the lateral geniculate nucleus (LGN) was assayed from the amplitude of potentials evoked in optic radiation by an electrical pulse applied to optic tract. Averaging of either individually or machine selected potentials, elicited at 0.3, 1.0, 20 or 50 Hz, in all cases showed a decrease in transmission ranging from 5–60 % in the period after saccadic eye movements made ad libitum. The suppression was greater in a patterned visual environment than in diffuse illumination, which in turn was greater than that occurring following saccades in the dark. Demonstration of the effect in darkness always required data averaging and never exceeded 20%. The effect was consistently greater in the magnocellular than parvocellular component. Suppression was often abruptly terminated and replaced by a facilitation of 5–15% about 100 msec after saccade detection. Comparable effects were observed for excitability of striate cortex tested by a stimulus pulse applied to optic radiation. In addition, sharply demarcated potentials inherently arising in LGN and striate cortex were found in association with saccades made even in total darkness. Neglecting a possible but dubious contribution from eye muscle proprioceptors, the experiments establish the existence of a centrally originating modulation of visual processing at both LGN and striate cortex in relation to saccadic eye movement in primates. This modulation may partially underlie the phenomenon of saccadic suppression and hasten the acquisition of a meaningful visual sample immediately following an ocular saccade. It remains uncertain as to how it may relate to similar or greater effects accompanying changes in alertness, or to fluctuations of unknown origin occurring sometimes semirhythmically at 0.05–0.03 Hz (Fig. 7).Supported by Grant NS 03606 and Contract 70-2279 from the National Institutes of Neurological Diseases and Stroke, National Institutes of Health and by Grant GB 7522X from the National Science Foundation. B.B.L. was also aided by a travel grant from the Wellcome Trust (U.K.) and H.S. received a travel grant from the International Brain Research Organization.