scholarly journals Comparison of superior colliculus and primary visual cortex in the coding of visual saliency

2014 ◽  
Vol 14 (10) ◽  
pp. 517-517 ◽  
Author(s):  
B. White ◽  
D. Berg ◽  
T. Ikeda ◽  
R. Levy ◽  
L. Itti ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Superior Colliculus ◽  
Primary Visual Cortex ◽  
Visual Saliency

scholarly journals Superior colliculus encodes visual saliency before the primary visual cortex

2017 ◽  
Vol 114 (35) ◽  
pp. 9451-9456 ◽  
Author(s):  
Brian J. White ◽  
Janis Y. Kan ◽  
Ron Levy ◽  
Laurent Itti ◽  
Douglas P. Munoz
Keyword(s):  
Visual Cortex ◽  
Superior Colliculus ◽  
Primary Visual Cortex ◽  
Visual Processing ◽  
Visual Saliency ◽  
Saliency Map ◽  
Stimulus Onset ◽  
Brain Areas ◽  
V1 Neurons ◽  
Processing Stream

Models of visual attention postulate the existence of a bottom-up saliency map that is formed early in the visual processing stream. Although studies have reported evidence of a saliency map in various cortical brain areas, determining the contribution of phylogenetically older pathways is crucial to understanding its origin. Here, we compared saliency coding from neurons in two early gateways into the visual system: the primary visual cortex (V1) and the evolutionarily older superior colliculus (SC). We found that, while the response latency to visual stimulus onset was earlier for V1 neurons than superior colliculus superficial visual-layer neurons (SCs), the saliency representation emerged earlier in SCs than in V1. Because the dominant input to the SCs arises from V1, these relative timings are consistent with the hypothesis that SCs neurons pool the inputs from multiple V1 neurons to form a feature-agnostic saliency map, which may then be relayed to other brain areas.

scholarly journals Spatial integration in mouse primary visual cortex

2013 ◽  
Vol 110 (4) ◽  
pp. 964-972 ◽  
Author(s):  
Agne Vaiceliunaite ◽  
Sinem Erisken ◽  
Florian Franzen ◽  
Steffen Katzner ◽  
Laura Busse
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Neural Circuits ◽  
Temporal Dynamics ◽  
Visual Saliency ◽  
Brain State ◽  
Inhibitory Interneurons ◽  
Spatial Integration ◽  
V1 Neurons ◽  
Contrast Normalization

Responses of many neurons in primary visual cortex (V1) are suppressed by stimuli exceeding the classical receptive field (RF), an important property that might underlie the computation of visual saliency. Traditionally, it has proven difficult to disentangle the underlying neural circuits, including feedforward, horizontal intracortical, and feedback connectivity. Since circuit-level analysis is particularly feasible in the mouse, we asked whether neural signatures of spatial integration in mouse V1 are similar to those of higher-order mammals and investigated the role of parvalbumin-expressing (PV+) inhibitory interneurons. Analogous to what is known from primates and carnivores, we demonstrate that, in awake mice, surround suppression is present in the majority of V1 neurons and is strongest in superficial cortical layers. Anesthesia with isoflurane-urethane, however, profoundly affects spatial integration: it reduces the laminar dependency, decreases overall suppression strength, and alters the temporal dynamics of responses. We show that these effects of brain state can be parsimoniously explained by assuming that anesthesia affects contrast normalization. Hence, the full impact of suppressive influences in mouse V1 cannot be studied under anesthesia with isoflurane-urethane. To assess the neural circuits of spatial integration, we targeted PV+ interneurons using optogenetics. Optogenetic depolarization of PV+ interneurons was associated with increased RF size and decreased suppression in the recorded population, similar to effects of lowering stimulus contrast, suggesting that PV+ interneurons contribute to spatial integration by affecting overall stimulus drive. We conclude that the mouse is a promising model for circuit-level mechanisms of spatial integration, which relies on the combined activity of different types of inhibitory interneurons.

scholarly journals Human blindsight is mediated by an intact geniculo-extrastriate pathway

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Sara Ajina ◽  
Franco Pestilli ◽  
Ariel Rokem ◽  
Christopher Kennard ◽  
Holly Bridge
Keyword(s):  
Magnetic Resonance Imaging ◽  
Visual Cortex ◽  
White Matter ◽  
Magnetic Resonance ◽  
Superior Colliculus ◽  
Lateral Geniculate Nucleus ◽  
Primary Visual Cortex ◽  
Resonance Imaging ◽  
Residual Vision ◽  
Weighted Magnetic Resonance Imaging

Although damage to the primary visual cortex (V1) causes hemianopia, many patients retain some residual vision; known as blindsight. We show that blindsight may be facilitated by an intact white-matter pathway between the lateral geniculate nucleus and motion area hMT+. Visual psychophysics, diffusion-weighted magnetic resonance imaging and fibre tractography were applied in 17 patients with V1 damage acquired during adulthood and 9 age-matched controls. Individuals with V1 damage were subdivided into blindsight positive (preserved residual vision) and negative (no residual vision) according to psychophysical performance. All blindsight positive individuals showed intact geniculo-hMT+ pathways, while this pathway was significantly impaired or not measurable in blindsight negative individuals. Two white matter pathways previously implicated in blindsight: (i) superior colliculus to hMT+ and (ii) between hMT+ in each hemisphere were not consistently present in blindsight positive cases. Understanding the visual pathways crucial for residual vision may direct future rehabilitation strategies for hemianopia patients.

scholarly journals Distinct “driving” versus “modulatory” influences of different visual corticothalamic pathways

2021 ◽  
Author(s):  
Megan A. Kirchgessner ◽  
Alexis D. Franklin ◽  
Edward M. Callaway
Keyword(s):  
Cerebral Cortex ◽  
Visual Cortex ◽  
Superior Colliculus ◽  
Primary Visual Cortex ◽  
Cortical Layer ◽  
Single Neurons ◽  
Visual Responses ◽  
Thalamic Nuclei ◽  
Visual Thalamus

AbstractHigher-order (HO) thalamic nuclei interact extensively with the cerebral cortex and are innervated by excitatory corticothalamic (CT) populations in layers 5 and 6. While these distinct CT projections have long been thought to have different functional influences on the HO thalamus, this has never been directly tested. By optogenetically inactivating different CT populations in the primary visual cortex (V1) of awake mice, we demonstrate that layer 5, but not layer 6, CT projections drive visual responses in the HO visual pulvinar, even while both pathways provide retinotopic, baseline excitation to their thalamic targets. Inactivating the superior colliculus also suppressed visual responses in the pulvinar, demonstrating that cortical layer 5 and subcortical inputs both contribute to HO visual thalamic activity - even at the level of putative single neurons. Altogether, these results indicate a functional division of driver and modulator CT pathways from V1 to the visual thalamus in vivo.

scholarly journals A Bioinspired Visual Saliency Model

2019 ◽  
Vol 37 (3) ◽  
pp. 503-508
Author(s):  
Ke Zhang ◽  
Xinbo Zhao ◽  
Rong Mo
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Visual Saliency ◽  
Saliency Map ◽  
Input Image ◽  
Visual Signals ◽  
Bottom Up ◽  
Saliency Model ◽  
Visual Saliency Model ◽  
Public Datasets

This paper presents a bioinspired visual saliency model. The end-stopping mechanism in the primary visual cortex is introduced in to extract features that represent contour information of latent salient objects such as corners, line intersections and line endpoints, which are combined together with brightness, color and orientation features to form the final saliency map. This model is an analog for the processing mechanism of visual signals along from retina, lateral geniculate nucleus(LGN)to primary visual cortex V1:Firstly, according to the characteristics of the retina and LGN, an input image is decomposed into brightness and opposite color channels; Then, the simple cell is simulated with 2D Gabor filters, and the amplitude of Gabor response is utilized to represent the response of complex cell; Finally, the response of an end-stopped cell is obtained by multiplying the response of two complex cells with different orientation, and outputs of V1 and LGN constitute a bottom-up saliency map. Experimental results on public datasets show that our model can accurately predict human fixations, and the performance achieves the state of the art of bottom-up saliency model.

scholarly journals The Timing and Neuroanatomy of Conscious Vision as Revealed by TMS-induced Blindsight

2014 ◽  
Vol 26 (7) ◽  
pp. 1507-1518 ◽  
Author(s):  
Christopher P. G. Allen ◽  
Petroc Sumner ◽  
Christopher D. Chambers
Keyword(s):  
Visual Cortex ◽  
Superior Colliculus ◽  
Primary Visual Cortex ◽  
Visual Stimuli ◽  
Stimulus Onset ◽  
Neural Basis ◽  
The Unconscious ◽  
Intermediate Period ◽  
Residual Capacity ◽  
Apparent Conflict

Following damage to the primary visual cortex, some patients exhibit “blindsight,” where they report a loss of awareness while retaining the ability to discriminate visual stimuli above chance. Transient disruption of occipital regions with TMS can produce a similar dissociation, known as TMS-induced blindsight. The neural basis of this residual vision is controversial, with some studies attributing it to the retinotectal pathway via the superior colliculus whereas others implicate spared projections that originate predominantly from the LGN. Here we contrasted these accounts by combining TMS with visual stimuli that either activate or bypass the retinotectal and magnocellular (R/M) pathways. We found that the residual capacity of TMS-induced blindsight occurs for stimuli that bypass the R/M pathways, indicating that such pathways, which include those to the superior colliculus, are not critical. We also found that the modulation of conscious vision was time and pathway dependent. TMS applied either early (0–40 msec) or late (280–320 msec) after stimulus onset modulated detection of stimuli that did not bypass R/M pathways, whereas during an intermediate period (90–130 msec) the effect was pathway independent. Our findings thus suggest a prominent role for the R/M pathways in supporting both the preparatory and later stages of conscious vision. This may help resolve apparent conflict in previous literature by demonstrating that the roles of the retinotectal and geniculate pathways are likely to be more nuanced than simply corresponding to the unconscious/conscious dichotomy.

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