RESUMEN

Abnormalities in visual exploration affect the daily lives of patients with schizophrenia. For example, scanpath length during free-viewing is shorter in schizophrenia. However, its origin and its relevance to symptoms are unknown. Here we investigate the possibility that abnormalities in eye movements result from abnormalities in visual or visuo-cognitive processing. More specifically, we examined whether such abnormalities reflect visual salience in schizophrenia. Eye movements of 82 patients and 252 healthy individuals viewing natural and/or complex images were examined using saliency maps for static images to determine the contributions of low-level visual features to salience-guided eye movements. The results showed that the mean value for orientation salience at the gazes of the participants with schizophrenia were higher than that of the healthy control subjects. Further analyses revealed that orientation salience defined by the L + M channel of the DKL color space is specifically affected in schizophrenia, suggesting abnormalities in the magnocellular visual pathway. By looking into the computational stages of the visual salience, we found that the difference between schizophrenia and healthy control emerges at the earlier stage, suggesting functional decline in early visual processing. These results suggest that visual salience is affected in schizophrenia, thereby expanding the concept of the aberrant salience hypothesis of psychosis to the visual domain.

Asunto(s)

RESUMEN

In a monopolistically competitive model with production externalities, where individuals voluntarily provide offsets which compensate for degradation of environmental quality caused by their income earning activities, this paper examines how an increase in the population size affects the equilibrium levels of environmental quality, offsets, and net contributions. Whether labor supply is institutionally constrained or not, as the population size increases, environmental quality decreases and converges to zero. However, since offsets increase and converge to the degradation rate of environmental quality, the carbon neutrality theorem holds: net contributions are zero. These results are independent of the specification of the utility function.

RESUMEN

Patients with damage to the primary visual cortex (V1) can respond correctly to visual stimuli in their lesion-affected visual field above the chance level, an ability named blindsight. Here, we present a protocol for making an animal model of blindsight in macaque monkeys. We describe the steps to perform pre-lesion training of monkeys on a visual task, followed by lesion surgery, post-lesion training, and evaluation of blindsight. This animal model can be used to investigate the source of visual awareness. For complete details on the use and execution of this protocol, please refer to Yoshida et al. (2008)1 and Takakuwa et al. (2021).2.

Asunto(s)

RESUMEN

Various eye movement abnormalities and impairments in visual information processing have been reported in patients with schizophrenia. Therefore, dysfunction of saccadic eye movements is a potential biological marker for schizophrenia. In the present study, we used a pharmacological model of schizophrenia symptoms in marmosets and compared the eye movement characteristics of marmosets during free-viewing, using an image set identical to those used for human studies. It contains natural and complex images that were randomly presented for 8 s. As a pharmacological model of schizophrenia symptoms, a subanesthetic dose of ketamine was injected intramuscularly for transient and reversible manipulation. Eye movements were recorded and compared under a ketamine condition and a saline condition as a control. The results showed that ketamine affected eye movement characteristics during free-viewing. Saccades amplitude and scanpath length were significantly reduced in the ketamine condition. In addition, the duration of saccades was longer under the ketamine condition than under the saline condition. A similar tendency was observed for the duration of fixations. The number of saccades and fixations tended to decrease in the ketamine condition. The peak saccades velocity also decreased after ketamine injection whereas there was no difference in the main sequence relationship between saccades amplitude and peak velocity. These results suggest that ketamine affected visual exploration but did not affect the oculomotor aspect of saccades in marmosets, consistent with studies in patients with schizophrenia. Therefore, we conclude that the subanesthetic dose of ketamine is a promising pharmacological model of schizophrenia symptoms in common marmosets and can be used in combination with free-viewing paradigms to establish "translatable markers" for schizophrenia in primates.

RESUMEN

Some patients with damage to the primary visual cortex (V1) exhibit visuomotor ability, despite loss of visual awareness, a phenomenon termed "blindsight". We review a series of studies conducted mainly in our laboratory on macaque monkeys with unilateral V1 lesioning to reveal the neural pathways underlying visuomotor transformation and the cognitive capabilities retained in blindsight. After lesioning, it takes several weeks for the recovery of visually guided saccades toward the lesion-affected visual field. In addition to the lateral geniculate nucleus, the pathway from the superior colliculus to the pulvinar participates in visuomotor processing in blindsight. At the cortical level, bilateral lateral intraparietal regions become critically involved in the saccade control. These results suggest that the visual circuits experience drastic changes while the monkey acquires blindsight. In these animals, analysis based on signal detection theory adapted to behavior in the "Yes-No" task indicates reduced sensitivity to visual targets, suggesting that visual awareness is impaired. Saccades become less accurate, decisions become less deliberate, and some forms of bottom-up attention are impaired. However, a variety of cognitive functions are retained such as saliency detection during free viewing, top-down attention, short-term spatial memory, and associative learning. These observations indicate that blindsight is not a low-level sensory-motor response, but the residual visual inputs can access these cognitive capabilities. Based on these results we suggest that the macaque model of blindsight replicates type II blindsight patients who experience some "feeling" of objects, which guides cognitive capabilities that we naïvely think are not possible without phenomenal consciousness.

Asunto(s)

RESUMEN

Visual selection in primates is intricately linked to eye movements, which are generated by a network of cortical and subcortical neural circuits. When visual selection is performed covertly, without foveating eye movements toward the selected targets, a class of fixational eye movements, called microsaccades, is still involved. Microsaccades are small saccades that occur when maintaining precise gaze fixation on a stationary point, and they exhibit robust modulations in peripheral cueing paradigms used to investigate covert visual selection mechanisms. These modulations consist of changes in both microsaccade directions and frequencies after cue onsets. Over the past two decades, the properties and functional implications of these modulations have been heavily studied, revealing a potentially important role for microsaccades in mediating covert visual selection effects. However, the neural mechanisms underlying cueing effects on microsaccades are only beginning to be investigated. Here we review the available causal manipulation evidence for these effects' cortical and subcortical substrates. In the superior colliculus (SC), activity representing peripheral visual cues strongly influences microsaccade direction, but not frequency, modulations. In the cortical frontal eye fields (FEF), activity only compensates for early reflexive effects of cues on microsaccades. Using evidence from behavior, theoretical modeling, and preliminary lesion data from the primary visual cortex and microstimulation data from the lower brainstem, we argue that the early reflexive microsaccade effects arise subcortically, downstream of the SC. Overall, studying cueing effects on microsaccades in primates represents an important opportunity to link perception, cognition, and action through unaddressed cortical-subcortical neural interactions. These interactions are also likely relevant in other sensory and motor modalities during other active behaviors.

Asunto(s)

RESUMEN

Patients with damage to the primary visual cortex (V1) lose visual awareness, yet retain the ability to perform visuomotor tasks, which is called "blindsight." To understand the neural mechanisms underlying this residual visuomotor function, we studied a non-human primate model of blindsight with a unilateral lesion of V1 using various oculomotor tasks. Functional brain imaging by positron emission tomography showed a significant change after V1 lesion in saccade-related visuomotor activity in the intraparietal sulcus area in the ipsi- and contralesional posterior parietal cortex. Single unit recordings in the lateral bank of the intraparietal sulcus (lbIPS) showed visual responses to targets in the contralateral visual field on both hemispheres. Injection of muscimol into the ipsi- or contralesional lbIPSs significantly impaired saccades to targets in the V1 lesion-affected visual field, differently from previous reports in intact animals. These results indicate that the bilateral lbIPSs contribute to visuomotor function in blindsight.

Asunto(s)

RESUMEN

Schizophrenia affects various aspects of cognitive and behavioural functioning. Eye movement abnormalities are commonly observed in patients with schizophrenia (SZs). Here we examined whether such abnormalities reflect an anomaly in inhibition of return (IOR), the mechanism that inhibits orienting to previously fixated or attended locations. We analyzed spatiotemporal patterns of eye movement during free-viewing of visual images including natural scenes, geometrical patterns, and pseudorandom noise in SZs and healthy control participants (HCs). SZs made saccades to previously fixated locations more frequently than HCs. The time lapse from the preceding saccade was longer for return saccades than for forward saccades in both SZs and HCs, but the difference was smaller in SZs. SZs explored a smaller area than HCs. Generalized linear mixed-effect model analysis indicated that the frequent return saccades served to confine SZs' visual exploration to localized regions. The higher probability of return saccades in SZs was related to cognitive decline after disease onset but not to the dose of prescribed antipsychotics. We conclude that SZs exhibited attenuated IOR under free-viewing conditions, which led to restricted scene scanning. IOR attenuation will be a useful clue for detecting impairment in attention/orienting control and accompanying cognitive decline in schizophrenia.

Asunto(s)

RESUMEN

Saccades are stereotypic behaviors whose investigation improves our understanding of how primate brains implement precise motor control. Furthermore, saccades offer an important window into the cognitive and attentional state of the brain. Historically, saccade studies have largely relied on macaques. However, the cortical network giving rise to the saccadic command is difficult to study in macaques because relevant cortical areas lie in deep sulci and are difficult to access. Recently, a New World monkey. the marmoset, has garnered attention as an alternative to macaques because of advantages including its smooth cortical surface. However, adoption of the marmoset for oculomotor research has been limited due to a lack of in-depth descriptions of marmoset saccade kinematics and their ability to perform psychophysical tasks. Here, we directly compare free-viewing and visually guided behavior of marmoset, macaque, and human engaged in identical tasks under similar conditions. In the video free-viewing task, all species exhibited qualitatively similar saccade kinematics up to 25° in amplitude although with different parameters. Furthermore, the conventional bottom-up saliency model predicted gaze targets at similar rates for all species. We further verified their visually guided behavior by training them with step and gap saccade tasks. In the step paradigm, marmosets did not show shorter saccade reaction time for upward saccades whereas macaques and humans did. In the gap paradigm, all species showed similar gap effect and express saccades. Our results suggest that the marmoset can serve as a model for oculomotor, attentional, and cognitive research while we need to be aware of their difference from macaque or human.NEW & NOTEWORTHY We directly compared the results of a video free-viewing task and visually guided saccade tasks (step and gap) among three different species: marmoset, macaque, and human. We found that all species exhibit qualitatively similar saccadic kinematics and saliency-driven saccadic behavior albeit with different parameters. Our results suggest that the marmoset possesses similar neural mechanisms to macaque and human for saccadic control, and it is an appropriate model to study neural mechanisms for active vision and attention.

Asunto(s)

RESUMEN

Microsaccades are systematically modulated by peripheral spatial cues, and these eye movements have been implicated in perceptual and motor performance changes in cueing tasks. However, an additional oculomotor factor that may also influence performance in these tasks, fixational eye position itself, has been largely neglected so far. Using precise eye tracking and real-time retinal-image stabilization, we carefully analyzed fixational eye position dynamics and related them to microsaccade generation during spatial cueing. As expected, during baseline fixation, microsaccades corrected for a foveal motor error away from the preferred retinal locus of fixation (the so-called ocular position "set point" of the oculomotor system). However, we found that this relationship was violated during a short period immediately after cue onset; a subset of cue-directed "express microsaccades" that were highly precise in time and direction, and that were larger than regular microsaccades, occurred. These movements, having <100-ms latencies from cue onset, were triggered when fixational eye position was already at the oculomotor set point when the cue appeared; they were thus error-increasing rather than error-decreasing. Critically, even when no microsaccades occurred, fixational eye position itself was systematically deviated toward the cue, again with ~100-ms latency, suggesting that the oculomotor system establishes a new set point at different postcue times. This new set point later switched to being away from the cue after ~200-300 ms. Because eye position alters the location of retinal images, our results suggest that both eye position and microsaccades can be associated with performance changes in spatial cueing tasks. NEW & NOTEWORTHY Covert spatial cueing tasks are a workhorse for studying cognitive processing in humans and monkeys, but gaze is not perfectly stable during these tasks. We found that minute fixational eye position changes, independent of the more studied microsaccades, are not random in cueing tasks and are thus not "averaged out" in analyses. These changes can additionally dictate microsaccade times. Thus, in addition to microsaccadic influences, retinal image changes associated with fixational eye position are relevant for performance in cueing tasks.

Asunto(s)

RESUMEN

The variety of microtubule arrays observed across different cell types should require a diverse group of proteins that control microtubule organization. Nevertheless, mainly because of the intrinsic propensity of microtubules to easily form bundles upon stabilization, only a small number of microtubule crosslinking proteins have been identified, especially in postmitotic cells. Among them is microtubule crosslinking factor 1 (MTCL1) that not only interconnects microtubules via its N-terminal microtubule-binding domain (N-MTBD), but also stabilizes microtubules via its C-terminal microtubule-binding domain (C-MTBD). Here, we comprehensively analyzed the assembly structure of MTCL1 to elucidate the molecular basis of this dual activity in microtubule regulation. Our results indicate that MTCL1 forms a parallel dimer not only through multiple homo-interactions of the central coiled-coil motifs, but also the most C-terminal non-coiled-coil region immediately downstream of the C-MTBD. Among these homo-interaction regions, the first coiled-coil motif adjacent to N-MTBD is sufficient for the MTCL1 function to crosslink microtubules without affecting the dynamic property, and disruption of this motif drastically transformed MTCL1-induced microtubule assembly from tight to network-like bundles. Notably, suppression of the homo-interaction of this motif inhibited the endogenous MTCL1 function to stabilize Golgi-associated microtubules that are essential for Golgi-ribbon formation. Because the microtubule-stabilizing activity of MTCL1 is completely attributed to C-MTBD, the present study suggests possible interplay between N-MTBD and C-MTBD, in which normal crosslinking and accumulation of microtubules by N-MTBD is essential for microtubule stabilization by C-MTBD.

Asunto(s)

RESUMEN

Patients with damage to the primary visual cortex (V1) demonstrate residual visual performance during laboratory tasks despite denying having a conscious percept. The mechanisms behind such performance, often called blindsight, are not fully understood, but the use of surgically-induced unilateral V1 lesions in macaque monkeys provides a useful animal model for exploring such mechanisms. For example, V1-lesioned monkeys localize stimuli in a forced-choice condition while at the same time failing to report awareness of identical stimuli in a yes-no detection condition, similar to human patients. Moreover, residual cognitive processes, including saliency-guided eye movements, bottom-up attention with peripheral non-informative cues, and spatial short-term memory, have all been demonstrated in these animals. Here we examined whether post-lesion residual visuomotor processing can be modulated by top-down task knowledge. We tested two V1-lesioned monkeys with a visually guided saccade task in which we provided an informative foveal pre-cue about upcoming target location. Our monkeys fixated while we presented a leftward or rightward arrow (serving as a pre-cue) superimposed on the fixation point (FP). After various cue-target onset asynchronies (CTOAs), a saccadic target (of variable contrast across trials) was presented either in the affected (contra-lesional) or seeing (ipsi-lesional) hemifield. Critically, target location was in the same hemifield that the arrow pre-cue pointed towards in 80% of the trials (valid-cue trials), making the cue highly useful for task performance. In both monkeys, correct saccade reaction times were shorter during valid than invalid trials. Moreover, in one monkey, the ratio of correct saccades towards the affected hemifield was higher during valid than invalid trials. We replicated both reaction time and correct ratio effects in the same monkey using a symbolic color cue. These results suggest that V1-lesion monkeys can use informative cues to localize stimuli in the contra-lesional hemifield, consistent with reports of a human blindsight subject being able to direct attention in cueing paradigms. Because the superior colliculus (SC) may contribute to residual visual capabilities after V1 lesions, and because this structure is important for controlling attentional resources, we hypothesize that our results reflect, among others, SC involvement in integrating top-down task knowledge for guiding orienting behavior.

RESUMEN

Inherent in visual scene analysis is a bottleneck associated with the need to sequentially sample locations with foveating eye movements. The concept of a 'saliency map' topographically encoding stimulus conspicuity over the visual scene has proven to be an efficient predictor of eye movements. Our work reviews insights into the neurobiological implementation of visual salience computation. We start by summarizing the role that different visual brain areas play in salience computation, whether at the level of feature analysis for bottom-up salience or at the level of goal-directed priority maps for output behaviour. We then delve into how a subcortical structure, the superior colliculus (SC), participates in salience computation. The SC represents a visual saliency map via a centre-surround inhibition mechanism in the superficial layers, which feeds into priority selection mechanisms in the deeper layers, thereby affecting saccadic and microsaccadic eye movements. Lateral interactions in the local SC circuit are particularly important for controlling active populations of neurons. This, in turn, might help explain long-range effects, such as those of peripheral cues on tiny microsaccades. Finally, we show how a combination of in vitro neurophysiology and large-scale computational modelling is able to clarify how salience computation is implemented in the local circuit of the SC.This article is part of the themed issue 'Auditory and visual scene analysis'.

Asunto(s)

RESUMEN

Microsaccades exhibit systematic oscillations in direction after spatial cueing, and these oscillations correlate with facilitatory and inhibitory changes in behavioral performance in the same tasks. However, independent of cueing, facilitatory and inhibitory changes in visual sensitivity also arise pre-microsaccadically. Given such pre-microsaccadic modulation, an imperative question to ask becomes: how much of task performance in spatial cueing may be attributable to these peri-movement changes in visual sensitivity? To investigate this question, we adopted a theoretical approach. We developed a minimalist model in which: (1) microsaccades are repetitively generated using a rise-to-threshold mechanism, and (2) pre-microsaccadic target onset is associated with direction-dependent modulation of visual sensitivity, as found experimentally. We asked whether such a model alone is sufficient to account for performance dynamics in spatial cueing. Our model not only explained fine-scale microsaccade frequency and direction modulations after spatial cueing, but it also generated classic facilitatory (i.e., attentional capture) and inhibitory [i.e., inhibition of return (IOR)] effects of the cue on behavioral performance. According to the model, cues reflexively reset the oculomotor system, which unmasks oscillatory processes underlying microsaccade generation; once these oscillatory processes are unmasked, "attentional capture" and "IOR" become direct outcomes of pre-microsaccadic enhancement or suppression, respectively. Interestingly, our model predicted that facilitatory and inhibitory effects on behavior should appear as a function of target onset relative to microsaccades even without prior cues. We experimentally validated this prediction for both saccadic and manual responses. We also established a potential causal mechanism for the microsaccadic oscillatory processes hypothesized by our model. We used retinal-image stabilization to experimentally control instantaneous foveal motor error during the presentation of peripheral cues, and we found that post-cue microsaccadic oscillations were severely disrupted. This suggests that microsaccades in spatial cueing tasks reflect active oculomotor correction of foveal motor error, rather than presumed oscillatory covert attentional processes. Taken together, our results demonstrate that peri-microsaccadic changes in vision can go a long way in accounting for some classic behavioral phenomena.

RESUMEN

Macaque monkeys with a unilateral lesion in V1 have been used as an animal model of blindsight. While objective proof of blindsight requires that the two aspects of blindsight (residual forced-choice localization and attenuated yes-no detection) should be tested under identical stimulus conditions using bias-free measures of sensitivity, these have not been attained in studies of nonhuman primates. Here we tested two macaque monkeys with a unilateral V1 lesion with two saccade tasks using identical stimuli: a forced-choice (FC) task and a yes-no (YN) task. An analysis based on signal detection theory revealed that sensitivity in the FC task was significantly higher than that in the YN task. Such dissociation of sensitivity between the two tasks was not observed when near-threshold visual stimuli were presented in the normal, unaffected hemifield. These results suggest that the V1-lesioned monkeys resemble the well-studied blindsight patient G.Y., whose visual experience per se was completely abolished.

Asunto(s)

RESUMEN

Recently the authors showed that a computational model of visual saliency could account for changes in gaze behavior of monkeys with damage in the primary visual cortex. Here we propose a neural prosthesis to restore eye gaze behavior by electrically stimulating the superior colliculus to drive visual attention. The saliency computational model is used to calculate the stimulation parameters from a real-time camera stream. Our simulations demonstrate that electrodes implanted in the superior colliculus at 1.0mm spacing are, in principle, able to recover specifically those visual attention behaviors which are lost when the primary visual cortex is damaged.

Asunto(s)

RESUMEN

"Blindsight" is a phenomenon whereby hemianopic patients with damage in the primary visual cortex (V1) are able to process visual information in their blind visual field. Two pathways that bypass the V1 may be responsible for this residual vision. The first pathway is the retinotectal pathway in which the superior colliculus in the midbrain receives direct retinal signals and sends them to the extrastriate cortex via the pulvinar. The second pathway is the geniculo-extrastriate pathway in which direct retinal input to the lateral geniculate nucleus is sent straight to the extrastriate cortex. Herein, I summarize evidence supporting the involvement of either pathway. The evidence was obtained from anatomical, neurophysiological, imaging, and behavioral studies carried out on macaque monkeys and humans. I emphasize three points: 1) crosstalk exists between the retinotectal pathway and the geniculo-extrastriate pathway, that is, the projection from the superficial layer of the superior colliculus to the koniocellular layer of the lateral geniculate nucleus; 2) three visual channels (the luminance in the magnocellular pathway, the red-green opponency in the parvocellular pathway, and the blue-yellow opponency in the koniocellular pathway) are not independent, as previously assumed; and 3) a global reorganization in the brain circuit occurs following the lesions of the V1 and subsequent recovery. Finally, I introduce a recent study that employed a saliency computational model to quantitatively evaluate the residual visual channels in blindsight monkeys during free-viewing behavior. Their findings suggest that plastic changes occur in the color-processing pathways.

Asunto(s)

RESUMEN

Patients with damage to primary visual cortex (V1) demonstrate residual performance on laboratory visual tasks despite denial of conscious seeing (blindsight) [1]. After a period of recovery, which suggests a role for plasticity [2], visual sensitivity higher than chance is observed in humans and monkeys for simple luminance-defined stimuli, grating stimuli, moving gratings, and other stimuli [3-7]. Some residual cognitive processes including bottom-up attention and spatial memory have also been demonstrated [8-10]. To date, little is known about blindsight with natural stimuli and spontaneous visual behavior. In particular, is orienting attention toward salient stimuli during free viewing still possible? We used a computational saliency map model to analyze spontaneous eye movements of monkeys with blindsight from unilateral ablation of V1. Despite general deficits in gaze allocation, monkeys were significantly attracted to salient stimuli. The contribution of orientation features to salience was nearly abolished, whereas contributions of motion, intensity, and color features were preserved. Control experiments employing laboratory stimuli confirmed the free-viewing finding that lesioned monkeys retained color sensitivity. Our results show that attention guidance over complex natural scenes is preserved in the absence of V1, thereby directly challenging theories and models that crucially depend on V1 to compute the low-level visual features that guide attention.

Asunto(s)

RESUMEN

Iron-copper cooperative catalysis is shown to be effective for an alkene-Grignard exchange reaction and alkylmagnesiation of alkynes. The Grignard exchange between terminal alkenes (RCH═CH(2)) and cyclopentylmagnesium bromide was catalyzed by FeCl(3) (2.5 mol %) and CuBr (5 mol %) in combination with PBu(3) (10 mol %) to give RCH(2)CH(2)MgBr in high yields. 1-Alkyl Grignard reagents add to alkynes in the presence of a catalyst system consisting of Fe(acac)(3), CuBr, PBu(3), and N,N,N',N'-tetramethylethylenediamine to give ß-alkylvinyl Grignard reagents. The exchange reaction and carbometalation take place on iron, whereas copper assists with the exchange of organic groups between organoiron and organomagnesium species through transmetalation with these species. Sequential reactions consisting of the alkene-Grignard exchange and the alkylmagnesiation of alkynes were successfully conducted by adding an alkyne to a mixture of the first reaction. Isomerization of Grignard reagents from 2-alkyl to 1-alkyl catalyzed by Fe-Cu also is applicable as the first 1-alkyl Grignard formation step.

RESUMEN

Previous reports on 'blindsight' have shown that some patients with lesions of the primary visual cortex (V1) could localize visual targets in their scotoma with hand and/or eye movements without visual awareness. A role of the retino-tectal pathway on residual vision has been proposed but the direct evidence for this still remains sparse. To examine this possibility, we inactivated the superior colliculus (SC) of unilateral V1-lesioned monkeys using microinjections of muscimol, and analysed the effects on visually guided saccades. Following muscimol injections into the contralesional SC, the monkeys performed the visually guided saccade task with relatively minor deficits. The effects of ipsilesional SC inactivation were more severe. After injections, the monkeys failed to localize the target within the visual field represented at the injection site on the SC map. The effects of ipsilesional SC inactivation may result from sensory deficits, motor deficits or a combination of both. To examine these possibilities, we tested the effects of SC inactivation on the motor system by investigating spontaneous saccades. After inactivation of the ipsilesional SC, spontaneous saccades toward the injection site were not abolished, suggesting that impairment of visually guided saccades following inactivation of the ipsilesional SC could not be explained solely by a motor deficit and was primarily due to a visual deficit, presumably by interfering with processing in the superficial layer. We conclude that the retino-tectal pathway plays an essential role in residual vision after V1 lesion. The results suggest that this pathway may be involved in mediating unconscious vision in blindsight patients.

Asunto(s)