Neural mechanisms for color perception in the primary visual cortex

2002 ◽  
Vol 12 (4) ◽  
pp. 426-432 ◽  
Author(s):  
R Shapley
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Wang ◽  
Chuanliang Han ◽  
Tian Wang ◽  
Weifeng Dai ◽  
Yang Li ◽  
...  

AbstractStimulus-dependence of gamma oscillations (GAMMA, 30–90 Hz) has not been fully understood, but it is important for revealing neural mechanisms and functions of GAMMA. Here, we recorded spiking activity (MUA) and the local field potential (LFP), driven by a variety of plaids (generated by two superimposed gratings orthogonal to each other and with different contrast combinations), in the primary visual cortex of anesthetized cats. We found two distinct narrow-band GAMMAs in the LFPs and a variety of response patterns to plaids. Similar to MUA, most response patterns showed that the second grating suppressed GAMMAs driven by the first one. However, there is only a weak site-by-site correlation between cross-orientation interactions in GAMMAs and those in MUAs. We developed a normalization model that could unify the response patterns of both GAMMAs and MUAs. Interestingly, compared with MUAs, the GAMMAs demonstrated a wider range of model parameters and more diverse response patterns to plaids. Further analysis revealed that normalization parameters for high GAMMA, but not those for low GAMMA, were significantly correlated with the discrepancy of spatial frequency between stimulus and sites’ preferences. Consistent with these findings, normalization parameters and diversity of high GAMMA exhibited a clear transition trend and region difference between area 17 to 18. Our results show that GAMMAs are also regulated in the form of normalization, but that the neural mechanisms for these normalizations might differ from those of spiking activity. Normalizations in different brain signals could be due to interactions of excitation and inhibitions at multiple stages in the visual system.


1998 ◽  
Vol 4 (4) ◽  
pp. 227-230 ◽  
Author(s):  
Tirin Moore ◽  
Hillary R. Rodman ◽  
Charles G. Gross

The visual function that survives damage to the primary visual cortex (V1) in humans is often unaccompanied by awareness. This type of residual vision, called “blindsight,” has raised considerable interest because it implies a separation of conscious from unconscious vision mechanisms. The monkey visual system has proven to be a useful model in elucidating the possible neural mechanisms of residual vision and blindsight in humans. Clear similarities, however, between the phenomenology of human and monkey residual vision have only recently become evident. This article summarizes parallels between residual vision in monkeys and humans with damage to V1. These parallels Include the tendency of the remaining vision to require forced-choice testing and the fact that more robust residual vision remains when V1 damage is sustained early in life. NEUROSCIENTIST 4:227–230


2019 ◽  
Author(s):  
Laura Lungu ◽  
Ryan Stewart ◽  
David P. Luke ◽  
Devin B. Terhune

AbstractA wealth of data suggests that psychedelic drugs elicit spontaneous perceptual states that resemble synaesthesia although it is unclear whether these different forms of synaesthesia share overlapping neural mechanisms. Multiple studies have shown that developmental and trained synaesthesia is characterized by selective hyperexcitability in primary visual cortex and it has been proposed that cortical hyperexcitability may contribute to induced and acquired synaesthesia. This study tested the prediction that a case of acquired synaesthesia (LW) would display selectively elevated primary visual cortex excitability, as reflected in lower transcranial magnetic stimulation (TMS) phosphene thresholds, but no difference in motor thresholds, relative to controls. In contrast to this prediction, LW’s phosphene threshold was well within the threshold range of controls. These results suggest that acquired synaesthesia is not characterized by atypical visual cortex excitability.


2020 ◽  
Author(s):  
Peichao Li ◽  
Anupam K. Garg ◽  
Li A. Zhang ◽  
Mohammad S. Rashid ◽  
Edward M. Callaway

AbstractStudies of color perception have led to mechanistic models of how signals from cone-opponent retinal ganglion cells are integrated to generate color appearance. But it is not known where or how these hypothesized mechanisms occur in the brain. Here we show that cone opponent signals transmitted from the retina to primary visual cortex (V1) are integrated through highly organized circuits within V1 to generate the color opponent mechanisms that underlie color appearance. Combining intrinsic signal optical imaging (ISI) and 2-photon calcium imaging (2PCI) at single cell resolution, we demonstrate cone-opponent functional domains (COFDs) that combine L/M cone-opponent and S/L+M cone-opponent signals in precisely the combinations predicted from psychophysical studies of color perception. These give rise to an orderly organization of hue preferences of the neurons within the COFDs and the generation of hue “pinwheels”. COFDs occupy regions corresponding to both high and low cytochrome oxidase intensity (“blobs” and “interblobs”) but have a bias toward blobs. Thus, neural circuits in the primary visual cortex establish the boundary conditions for color opponency and unique hues.One Sentence SummaryCone-opponent functional domains generate color opponent functional architecture in primary visual cortex.


2021 ◽  
Author(s):  
Henry Railo ◽  
Mikko Hurme

The visual pathways that bypass the primary visual cortex (V1) are often assumed to support visually guided behavior in humans in the absence of conscious vision. This conclusion is largely based on findings on patients: V1 lesions cause blindness but sometimes leave some visually guided behaviors intact—this is known as blindsight. With the aim of examining how well the findings on blindsight patients generalize to neurologically healthy individuals, we review studies which have tried to uncover transcranial magnetic stimulation (TMS) induced blindsight. In general, these studies have failed to demonstrate a completely unconscious blindsight-like capacity in neurologically healthy individuals. A possible exception to this is TMS-induced blindsight of stimulus presence or location. Because blindsight in patients is often associated with some form of introspective access to the visual stimulus, and may be associated with neural reorganization, we suggest that rather than revealing a dissociation between neural mechanisms of behavior and conscious seeing, blindsight may reflect preservation or partial recovery of conscious visual perception after the lesion.


Author(s):  
Robert Shapley

Color perception in macaque monkeys and humans depends on the visually evoked activity in three cone photoreceptors and on neuronal post-processing of cone signals. Neuronal post-processing of cone signals occurs in two stages in the pathway from retina to the primary visual cortex. The first stage, in in P (midget) ganglion cells in the retina, is a single-opponent subtractive comparison of the cone signals. The single-opponent computation is then sent to neurons in the Parvocellular layers of the Lateral Geniculate Nucleus (LGN), the main visual nucleus of the thalamus. The second stage of processing of color-related signals is in the primary visual cortex, V1, where multiple comparisons of the single-opponent signals are made. The diversity of neuronal interactions in V1cortex causes the cortical color cells to be subdivided into classes of single-opponent cells and double-opponent cells. Double-opponent cells have visual properties that can be used to explain most of the phenomenology of color perception of surface colors; they respond best to color edges and spatial patterns of color. Single opponent cells, in retina, LGN, and V1, respond to color modulation over their receptive fields and respond best to color modulation over a large area in the visual field.


Sign in / Sign up

Export Citation Format

Share Document