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The visual pathways that guide actions do not necessarily mediate conscious perception. Patients with primary visual cortex (V1) damage lose conscious perception but often retain unconscious abilities (e.g. blindsight). Here, we asked if saccade accuracy and post-saccadic following responses (PFRs) that automatically track target motion upon saccade landing are retained when conscious perception is lost. We contrasted these behaviors in the blind and intact-fields of 11 chronic V1-stroke patients, and in 8 visually-intact controls. Saccade accuracy was relatively normal in all cases. Stroke patients also had normal PFR in their intact-fields, but no PFR in their blind-fields. Thus, V1 damage did not spare the unconscious visual processing necessary for automatic, post-saccadic smooth eye movements. Importantly, visual training that recovered motion perception in the blind-field did not restore the PFR, suggesting a clear dissociation between pathways mediating perceptual restoration and automatic actions in the V1-damaged visual system.

Responses of midbrain dopamine (DA) neurons reflecting expected reward from sensory cues are critical for reward-based associative learning. However, critical pathways by which reward-related visual information is relayed to DA neurons remain unclear. To address this question, we investigated Pavlovian conditioning in macaque monkeys with unilateral primary visual cortex (V1) lesions (an animal model of ‘blindsight’). Anticipatory licking responses to obtain juice drops were elicited in response to visual conditioned stimuli (CS) in the affected visual field. Subsequent pharmacological inactivation of the superior colliculus (SC) suppressed the anticipatory licking. Concurrent single unit recordings indicated that DA responses reflecting the reward expectation could be recorded in the absence of V1, and that these responses were also suppressed by SC inactivation. These results indicate that the subcortical visual circuit can relay reward-predicting visual information to DA neurons and integrity of the SC is necessary for visually-elicited classically conditioned responses after V1 lesion. DOI: http://dx.doi.org/10.7554/eLife.24459.001, eLife digest To survive and thrive, animals must learn to approach cues in their environment that are likely to lead to a desirable outcome and avoid those that might lead them to harm. A group of brain regions known as the midbrain dopamine system helps many animals to achieve this. Dopamine is the brain’s reward signal. Cues that predict rewards, such as the sight or smell of food, activate midbrain dopamine neurons. However, the details of this process remained unclear. Takakuwa et al. have now examined how visual information that signals reward reaches the midbrain dopamine neurons. The anatomy of the visual system suggests two main possibilities. Information may travel directly from the eyes to an area of the midbrain called the superior colliculus, and then onto the dopamine neurons. Alternatively, information may travel to the midbrain indirectly via a pathway that includes additional processing in the brain’s outer layer, the visual cortex. To distinguish between these routes, Takakuwa et al. studied monkeys in which the indirect pathway via the visual cortex had been damaged. Some people with damage to this pathway have a disorder called blindsight. They are able to detect the movement or location of stimuli, but they cannot consciously see those stimuli. The monkeys with damage to visual cortex were able to learn that an image on a screen predicted the delivery of fruit juice. After repeated trials, the monkeys began to lick the spout dispensing the juice whenever the image appeared, even if no juice was delivered. The monkeys’ midbrain dopamine neurons also sent more signals in response to the images, and showed greater activity when the images predicted large rewards than small ones. Takakuwa et al. next inactivated the superior colliculus with a drug and showed that this prevented both the licking behavior and the increased signaling. Together the findings show that visual information about potential rewards can reach midbrain dopamine neurons via a direct route through the superior colliculus, without needing to pass via the visual cortex. The next step is to determine how and when the visual cortex may get involved in this process to help animals maximize rewards. DOI: http://dx.doi.org/10.7554/eLife.24459.002

Many believe that humans can ‘perceive unconsciously’ – that for weak stimuli, briefly presented and masked, above-chance discrimination is possible without awareness. Interestingly, an online survey reveals that most experts in the field recognize the lack of convincing evidence for this phenomenon, and yet they persist in this belief. Using a recently developed bias-free experimental procedure for measuring subjective introspection (confidence), we found no evidence for unconscious perception; participants’ behavior matched that of a Bayesian ideal observer, even though the stimuli were visually masked. This surprising finding suggests that the thresholds for subjective awareness and objective discrimination are effectively the same: if objective task performance is above chance, there is likely conscious experience. These findings shed new light on decades-old methodological issues regarding what it takes to consider a neurobiological or behavioral effect to be 'unconscious,' and provide a platform for rigorously investigating unconscious perception in future studies. DOI: http://dx.doi.org/10.7554/eLife.09651.001, eLife digest In the 1980s, psychologists made an unexpected discovery while working with individuals who had become blind after sustaining damage to areas of the brain required for vision. These individuals could respond correctly to questions about the shape and location of objects in their visual field, even though they could no longer see the objects. This phenomenon became known as 'blindsight', and it is regarded as a classic example of perception in the absence of conscious awareness. Many researchers who study consciousness believe that everyone is capable of subliminal or unconscious perception: that is, of detecting and processing stimuli without being consciously aware of them. However, studies investigating this phenomenon have produced contradictory results. Peters and Lau have now tested unconscious perception directly, using a recently developed method that overcomes some of the problems faced by previous studies. Human volunteers took part in several trials, in which they were shown two images. Each image was ‘masked’ to prevent the volunteers from consciously registering them. After each image was shown, the volunteers had to state whether a patch of gray and white stripes in the masked image was tilted to the left or to the right. However, one of the two images did not include a gray and white patch. After seeing both images in a trial, the volunteers also had to indicate which of their answers they were most confident about. If the volunteers could perceive the patches without being consciously aware of doing so, their response should show two features. The volunteers should correctly state the tilt direction of the stripes more often than would be expected if they were guessing at random. However, they should also feel no more confident in their responses for the images that did feature a striped patch than for the ‘no patch’ ones. Peters and Lau found no such evidence of unconscious perception. Nevertheless, the volunteers were consistently better at correctly stating the direction the stripes were tilted in than their confidence ratings would suggest. Does this indicate some degree of perception without awareness? Peters and Lau argue that it does not, because a computer model designed to perform the task showed a similar level of performance to the volunteers. These findings suggest that previous reports of unconscious perception may have been contaminated by the problems that Peters and Lau controlled for, and that perhaps unconscious perception doesn’t occur in people without brain damage. Researchers will now need to do more studies using similar approaches to determine whether observers without brain damage can truly experience unconscious perception, and how such unconscious perception might be represented in the brain. DOI: http://dx.doi.org/10.7554/eLife.09651.002

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. DOI: http://dx.doi.org/10.7554/eLife.08935.001, eLife digest Visual information from our eyes projects to a region at the back of the brain called the primary visual cortex, which is where the information is processed to allow us to see the world around us. If a person suffers a stroke that affects this primary visual cortex, he or she can become blind on one side. However, some people can still detect images within this ‘blind’ area, even if they are not consciously aware of it. This phenomenon is known as ‘blindsight’, but it remains unclear which pathways and structures in the brain might allow this information to be detected. Ajina et al. have now examined the brains of a large group of patients with damage to the visual cortex. The results for the patients with blindsight were compared to those without, and to a group of sighted control participants. This analysis identified a pathway that seems to underlie blindsight. This pathway (which runs between an area of the brain called the lateral geniculate nucleus and another called the motion area hMT+) was present in all patients with blindsight, but was missing or disrupted in those patients without blindsight. Ajina et al. then examined other pathways that had previously been suggested to support blindsight and revealed that they were unlikely to do so. This is because the suggested connections were not identifiable in all patients with blindsight, and were often intact in those patients without blindsight. So far, this work has addressed the structure of the pathways rather than their activity. Future work will attempt to determine whether it is possible to strengthen such pathways to improve visual ability. DOI: http://dx.doi.org/10.7554/eLife.08935.002

Vision depends on the brain as well as on the eyes. Almost all information from the eyes travels to a brain region called the primary visual cortex. This large expanse of tissue at the back of the brain contains a detailed map of the visual world. Adults who suffer damage to part of the primary visual cortex become blind in the corresponding area of visual space, a phenomenon known as cortical blindness. Yet, adults with cortical blindness can also experience ‘blindsight’: they can still point correctly to bright, moving images, even though they claim they cannot see them. One of the roles of primary visual cortex is to act as a gateway to other, ‘higher’ visual areas of the brain. These regions process the input they receive from the primary visual cortex to generate a rich and coherent visual representation. But how do adults with blindsight, in whom the major gateway from the eyes to higher visual areas has been damaged, still manage to respond to visual stimuli? By chance, Bridge et al. discovered a monkey whose unusual brain anatomy provides clues as to why this is possible. The monkey behaved much like its peers, leaping between the perches of its enclosure with ease. But when Bridge et al. tried to train the animal on a visual task, it proved unable to learn like the other monkeys. A brain scan revealed that it had almost no primary visual cortex, probably because of an abnormality that arose early in development. Further studies of the monkey’s brain showed that the other structures involved in visual processing were in their usual places and were of normal size. Connections from the eyes to higher visual areas that bypass the primary visual cortex were normal, but were no stronger than in other monkeys. In fact, areas beyond the primary visual cortex showed no fundamental changes in how they processed visual information. The brain of this monkey had thus adapted to early loss of the major gateway from the eyes to higher visual cortex. Visual areas of the brain beyond the primary visual cortex continued to work as normal, helping to minimize vision loss. Because the visual brain differs little between primates, this discovery could also benefit patients with blindsight. It suggests that targeting higher visual areas could further improve vision in patients with damage to the primary visual cortex.