Electrical microstimulation of the striate cortex (area V1) in monkeys delays the execution of saccadic eye movements generated to a visual target located in the receptive field of the stimulated neurons. We have argued that this effect is because of disruption of the visual signal transmitted along the geniculostriate pathway. The delivery of electrical stimulation to V1 evokes a punctate light or dark phosphene in human subjects. If electrical stimulation of V1 in monkeys evokes a light or dark phosphene, then one might expect that the delay effect might vary according to whether monkeys are required to detect a light or a dark visual target. For instance, if the stimulation is activating V1 elements coding for a light visual stimulus but not a dark visual stimulus then stimulation may delay saccades generated to a light target but not to a dark target. We tested this idea by having monkeys generate saccadic eye movements to light or dark visual targets immediately after the stimulation was delivered to V1. We found that the delay effect induced by stimulation varied with target contrast, but remained invariant to whether a bright or dark visual target was presented in the receptive field of the stimulated neurons. The significance of these results is discussed with regard to using monkeys to develop a visual prosthesis for the blind.
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http://dx.doi.org/10.1007/s00221-005-2306-x | DOI Listing |
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