Blindsight: insights from neuronal responses in macaque V4 after V1 injury

J Schmiedt1, A Peters2, R Saunders2, A Maier3, D Leopold2, M Schmid1

1Schmid Lab, Ernst Strüngmann Institute (ESI), Germany
2Cognitive Neurophysiology and Imaging, National Institute of Mental Health, MD, United States
3Department of Psychology, Vanderbilt University, TN, United States
Contact: joscha.schmiedt@esi-frankfurt.de

Patients with V1 lesions can retain a remarkable capacity for detecting visual stimuli while their perceptual visual experience is lost (“blindsight”). The question to what extent ventral-stream area V4 participates in blindsight by processing V1-independent information has so far remained controversial: Temporary cooling of macaque V1 virtually abolished neuronal activity in V4 (Girard et al., 1991, Neuroreport, 2, 81-84). In contrast, weak yet reliable fMRI responses were elicited by visual stimulation in the lesion-affected part of the visual field (scotoma) in monkeys with permanent V1 injury (Schmid et al, 2010, Nature, 466, 373-377). Here, using chronically implanted intracortical electrode arrays, we recorded neural activity in V4 before and after targeted V1 aspiration lesions. Following the V1 lesion, most V4 sites ceased to respond to visual stimulation in the scotoma. Nevertheless, a minority of sites showed weak but significant multi-unit responses to visual stimuli presented in the scotoma and exhibited motion-sensitivity. Local field potential analysis revealed power decreases in the gamma and increases in the beta range, possibly reflecting changes in feedforward and feedback signaling. In conclusion, our results indicate a V4 contribution to motion detection in blindsight that may be mediated by unmasking of motion-related processes.

Up Home