Visual aftereffects and the consequences of visual system lesions on their perception in the rhesus monkey

1994 ◽  
Vol 11 (4) ◽  
pp. 643-665 ◽  
Author(s):  
Peter H. Schiller ◽  
Robert P. Dolan
Keyword(s):  
Rhesus Monkey ◽  
Visual System ◽  
Lateral Geniculate Nucleus ◽  
Striate Cortex ◽  
Luminance Contrast ◽  
Repeated Exposure ◽  
Lateral Geniculate ◽  
Central Factors

AbstractThis study examined the consequences of visual system lesions on visual aftereffects produced by achromatic stimuli of various luminance contrasts and chromatic stimuli of various wavelength compositions. The effects of repeated exposure to such adapting stimuli were assessed using probes whose luminance contrast and wavelength composition were systematically varied using both detection and discrimination paradigms. Interocular tests revealed that both peripheral and central mechanisms contribute to the visual aftereffects produced by the adapting stimulus arrays used in this study. Contrary to the hypothesis according to which the midget system of the retina is the conveyor of visual afterimages, we found that blocking this system with lesions of parvocellular lateral geniculate nucleus, through which the midget cells make their way to the striate cortex in primates, did not eliminate the visual aftereffects. It appears therefore that the parasol system of the retina, which courses through the magnocellular layers of the lateral geniculate nucleus to cortex, can convey the necessary signals for the generation of visual aftereffects. Lesions of areas V4 and MT did not have significant effects on the visual aftereffects studied suggesting that the central factors that contribute to the visual aftereffects occur either already in area VI or are conveyed to higher centers through regions other than areas V4 and MT.

Organization of Binocular Pathways: Modeling and Data Related to Rivalry

1991 ◽  
Vol 3 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Sidney R. Lehky ◽  
Randolph Blake
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Binocular Rivalry ◽  
Striate Cortex ◽  
Reciprocal Inhibition ◽  
Lateral Geniculate ◽  
Layer 4 ◽  
Inhibitory Coupling ◽  
Binocular Matching

It is proposed that inputs to binocular cells are gated by reciprocal inhibition between neurons located either in the lateral geniculate nucleus or in layer 4 of striate cortex. The strength of inhibitory coupling in the gating circuitry is modulated by layer 6 neurons, which are the outputs of binocular matching circuitry. If binocular inputs are matched, the inhibition is modulated to be weak, leading to fused vision, whereas if the binocular inputs are unmatched, inhibition is modulated to be strong, leading to rivalrous oscillations. These proposals are buttressed by psychophysical experiments measuring the strength of adaptational aftereffects following exposure to an adapting stimulus visible only intermittently during binocular rivalry.

Monocular enucleation reduces immunoreactivity to the calcium-binding protein calbindin 28 kD in the Rhesus monkey lateral geniculate nucleus

1992 ◽  
Vol 9 (5) ◽  
pp. 471-482 ◽  
Author(s):  
R. Ranney Mize ◽  
Qian Luo ◽  
Margarete Tigges
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Optical Density ◽  
Calcium Binding ◽  
Striate Cortex ◽  
Binding Protein ◽  
Visual Deprivation ◽  
Calcium Binding Protein ◽  
Monocular Enucleation ◽  
Lateral Geniculate ◽  
Antibody Labeling

AbstractThe calcium-binding proteins calbindin (CaBP) and parvalbumin (PV) are important in regulating intracellular calcium in brain cells. PV immunoreactivity is reduced by enucleation in the lateral geniculate nucleus (LGN) and by enucleation and visual deprivation in the striate cortex of adult monkeys. The effects of enucleation and visual deprivation on CaBP immunoreactivity in the LGN are not known. We therefore have studied cells and neuropil in the LGN that are labeled by antibodies to CaBP in normal and visually deprived Rhesus monkeys to determine if there is an effect on this calcium-binding protein. One group of monkeys had one eye removed 2 weeks to 4.3 years before sacrifice. A second group had one eye occluded with opaque lenses from infancy without enucleation. A final group had one eye occluded long-term followed by short-term enucleation 2 weeks before sacrifice.In normal monkeys, CaBP-immunoreactive neurons were found throughout the LGN. They were sparsely distributed within the six main laminae, and more densely distributed within layer S and the interlaminar zones (ILZ). The labeled ILZ neurons had a distinct morphology, with fusiform somata and elaborate dendritic trees that were confined primarily to the ILZ. Most CaBP-labeled neurons in the main layers had dendrites that radiated in all directions from the soma. ILZ and main layer cells labeled by CaBP thus probably represent two different cell types.Monocular enucleation with or without occlusion produced a significant reduction in antibody labeling in the deafferented laminae. Field measures revealed an average 11.5% reduction in optical density in each deafferented lamina compared to its adjacent, nondeprived layer. The differences in field optical density between deprived and nondeprived layers were statistically significant. CaBP neurons were still visible, but the optical density of antibody labeling in these cells also was reduced. Occlusion without enucleation had no effect. Thus, deafferentation, but not light deprivation, reduces concentrations of CaBP in monkey LGN. This effect is different than that seen in striate cortex of adult monkeys, where visual deprivation as well as enucleation alters CaBP immunoreactivity.

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