Neurochemical changes in the primate lateral geniculate nucleus following lesions of striate cortex in infancy and adulthood: implications for residual vision and blindsight

2021 ◽  
Author(s):  
Nafiseh Atapour ◽  
Katrina H. Worthy ◽  
Marcello G. P. Rosa
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Striate Cortex ◽  
Lateral Geniculate ◽  
Residual Vision ◽  
Neurochemical Changes

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.

scholarly journals Feedback from V1 and inhibition from beyond the classical receptive field modulates the responses of neurons in the primate lateral geniculate nucleus

2002 ◽  
Vol 19 (5) ◽  
pp. 583-592 ◽  
Author(s):  
BEN S. WEBB ◽  
CHRIS J. TINSLEY ◽  
NICK E. BARRACLOUGH ◽  
ALEXANDER EASTON ◽  
AMANDA PARKER ◽  
...  
Keyword(s):  
Receptive Field ◽  
Firing Rate ◽  
Lateral Geniculate Nucleus ◽  
Visual Information ◽  
Striate Cortex ◽  
Temporal Frequency ◽  
Optimal Size ◽  
Marmoset Monkey ◽  
Lateral Geniculate ◽  
Classical Receptive Field

It is well established that the responses of neurons in the lateral geniculate nucleus (LGN) can be modulated by feedback from visual cortex, but it is still unclear how cortico-geniculate afferents regulate the flow of visual information to the cortex in the primate. Here we report the effects, on the gain of LGN neurons, of differentially stimulating the extraclassical receptive field, with feedback from the striate cortex intact or inactivated in the marmoset monkey, Callithrix jacchus. A horizontally oriented grating of optimal size, spatial frequency, and temporal frequency was presented to the classical receptive field. The grating varied in contrast (range: 0–1) from trial to trial, and was presented alone, or surrounded by a grating of the same or orthogonal orientation, contained within either a larger annular field, or flanks oriented either horizontally or vertically. V1 was ablated to inactivate cortico-geniculate feedback. The maximum firing rate of LGN neurons was greater with V1 intact, but was reduced by visually stimulating beyond the classical receptive field. Large horizontal or vertical annular gratings were most effective in reducing the maximum firing rate of LGN neurons. Magnocellular neurons were most susceptible to this inhibition from beyond the classical receptive field. Extraclassical inhibition was less effective with V1 ablated. We conclude that inhibition from beyond the classical receptive field reduces the excitatory influence of V1 in the LGN. The net balance between cortico-geniculate excitation and inhibition from beyond the classical receptive field is one mechanism by which signals relayed from the retina to V1 are controlled.

A functional role of cholinergic innervation to neurons in the cat visual cortex

1987 ◽  
Vol 58 (4) ◽  
pp. 765-780 ◽  
Author(s):  
H. Sato ◽  
Y. Hata ◽  
H. Masui ◽  
T. Tsumoto
Keyword(s):  
Electrical Stimulation ◽  
Lateral Geniculate Nucleus ◽  
Cortical Neurons ◽  
Striate Cortex ◽  
Cholinergic Innervation ◽  
Neuron Activity ◽  
Visual Responses ◽  
Stimulus Movement ◽  
Lateral Geniculate ◽  
Stimulation Of

1. Effects of microionophoretic application of acetylcholine (ACh) and its antagonists on neuronal responses to visual stimuli and to electrical stimulation of the lateral geniculate nucleus were studied in the cat striate cortex. 2. Responses elicited visually and electrically were facilitated by ACh in 74% of the cells tested, whereas the responses were suppressed in 16%. These ACh effects were blocked by a muscarinic antagonist, atropine, but not by a nicotinic antagonist, hexamethonium, indicating that the ACh effects are mediated through muscarinic receptors. A single application of atropine suppressed visual responses of cells facilitated by ACh, whereas it enhanced those of cells inhibited by ACh, suggesting that endogenous ACh may tonically modulate visual responsivity of cortical neurons. 3. In most cells with the facilitatory ACh effect, responses with single spikes to the electrical stimulation became more consistent, often with double spikes, during the ACh application. The suppressive effects of ACh were noted most often in cells with a longer response latency to electrical stimulation of lateral geniculate nucleus. 4. In most of the facilitated cells the spontaneous activity remained null or very low during ACh application, in spite of marked enhancement of visual responses, suggesting that ACh may improve the signal-to-noise ratio (S/N) of cortical neuron activity. To confirm this suggestion, we calculated a S/S + N index by counting the total number of spikes in the responses (S) and that in peristimulus time histogram (S + N) and found that it was improved during the ACh application in about a half of the cells, whereas it became worse in about one-fifth. 5. In most of the facilitated cells, ACh enhanced visual responses not only to optimal but also to nonoptimal stimuli, resulting in no improvement or even worsening of the orientation selectivity. This was also the case in the selectivity of direction of stimulus movement. 6. The laminar location of the facilitated cells was biased toward layers V and VI of the cortex, although they also made up the majority in layers II + III and about half the tested cells in layers IVab and IVc. 7. In the light of recent understanding of cortical circuitry, these results suggest that the cholinergic innervation to cortical neurons may play a role in improvement of the S/N ratio of information processing in the striate cortex and in facilitation of sending processed informations to other visual centers.

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.

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