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Debra W. Soh, M.A., Keith A. Schneider; Functionally imaging the magno- and parvocellular layers of the human LGN during binocular rivalry. Journal of Vision 2013;13(9):548. doi: https://doi.org/10.1167/13.9.548.
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© ARVO (1962-2015); The Authors (2016-present)
Introduction. Binocular rivalry occurs when conflicting images are presented to the eyes dichoptically. Rather than being perceived as one cohesive image, the two images compete for perceptual dominance, resulting in the images alternating in perceptual awareness. Neural explanations for this phenomenon have been debated; our interest was to determine the involvement of the magnocellular (M) and parvocellular (P) processing streams in rivalry. The lateral geniculate nucleus (LGN) is involved in dominance and suppression of visual input, consists of two ventral M layers and four dorsal P layers, and is the only place in the brain where these streams are spatially disjoint. Previous research has shown that activity in the LGN layers innervated by the suppressed eye is also suppressed during rivalry, but it is not clear whether both M and P streams are equally involved. Methods. Participants were scanned using a Siemens 3T MRI scanner. Functional EPI data were registered to a mean series of high-resolution proton density weighted images on which it is possible to measure the boundaries of the LGN and thus localize the M and P layers. Stimuli were presented through an Avotec binocular goggle system that allowed independent stimulation of each eye. The rivalrous stimuli were two rotating (1 Hz period) discs of high-contrast sinusoidal gratings that varied with regards to colour (red vs. green) and direction of rotation. Subjects held down a button to indicate which of the two stimuli was currently being perceived. Event-related averages were calculated from the functional data within the LGN. Results. The activation strengths of the M and P streams were compared. Both streams were found to participate equally in rivalry. Discussion. These results have implications for potential treatments for clinical disorders that result from M-cell deficits (e.g., dyslexia) and attentional disorders (e.g., attention deficit hyperactivity disorder, neglect syndromes).
Meeting abstract presented at VSS 2013
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