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For millennia, people have used “averted vision” to improve their detection of faint celestial objects, a technique first documented around 325 BCE. Yet, no studies have assessed gaze location during averted vision to determine what pattern best facilitates perception. Here, we characterized averted vision while recording eye-positions of dark-adapted human participants, for the first time. We simulated stars of apparent magnitudes 3.3 and 3.5, matching their brightness to Megrez (the dimmest star in the Big Dipper) and Tau Ceti. Participants indicated whether each star was visible from a series of fixation locations, providing a comprehensive map of detection performance in all directions. Contrary to prior predictions, maximum detection was first achieved at ~8° from the star, much closer to the fovea than expected from rod-cone distributions alone. These findings challenge the assumption of optimal detection at the rod density peak and provide the first systematic assessment of an age-old facet of human vision.

Fixational eye movements (FEMs), including microsaccades, drift, and tremor, shift our eye position during ocular fixation, producing retinal motion that is thought to help visibility by counteracting neural adaptation to unchanging stimulation. Yet, how each FEM type influences this process is still debated. Recent studies found little to no relationship between microsaccades and visual perception of spatial frequencies (SF). However, these conclusions were based on coarse analyses that make it hard to appreciate the actual effects of microsaccades on target visibility as a function of SF. Thus, how microsaccades contribute to the visibility of stimuli of different SFs remains unclear. Here, we asked how the visibility of targets of various SFs changed over time, in relationship with concurrent microsaccade production. Participants continuously reported on changes in target visibility, allowing us to time-lock ongoing changes in microsaccade parameters to perceptual transitions in visibility. Microsaccades restored/increased the visibility of low SF targets more efficiently than that of high SF targets. Yet, microsaccade rates rose before periods of increased visibility, and dropped before periods of diminished visibility, for all the SFs tested, suggesting that microsaccades boosted target visibility across a wide range of SFs. Our data also indicate that visual stimuli fade/become harder to see less often in the presence of microsaccades. In addition, larger microsaccades restored/increased target visibility more effectively than smaller microsaccades. These combined results support the proposal that microsaccades enhance visibility across a broad variety of SFs.

Most research connecting task performance and neural activity to date has been conducted in laboratory conditions. Thus, field studies remain scarce, especially in extreme conditions such as during real flights. Here, we investigated the effects of flight procedures of varied complexity on the in-flight EEG activity of military helicopter pilots. Flight procedural complexity modulated the EEG power spectrum: highly demanding procedures (i.e., takeoff and landing) were associated with higher EEG power in the higher frequency bands, whereas less demanding procedures (i.e., flight exercises) were associated with lower EEG power over the same frequency bands. These results suggest that EEG recordings may help to evaluate an operator's cognitive performance in challenging real-life scenarios, and thus could aid in the prevention of catastrophic events.

Fixational eye movements (FEMs; including microsaccades, drift and tremor) are thought to improve visibility during fixation by thwarting neural adaptation to unchanging stimuli, but how the different FEM types influence this process is a matter of debate. Attempts to answer this question have been hampered by the failure to distinguish between the prevention of fading (where fading is blocked before it happens in the first place) and the reversal of fading (where vision is restored after fading has already occurred). Because fading during fixation is a detriment to clear vision, the prevention of fading, which avoids visual degradation before it happens, is a more desirable scenario than improving visibility after fading has occurred. Yet previous studies have not examined the role of FEMs in the prevention of fading, but have focused on visual restoration instead. Here we set out to determine the differential contributions and efficacies of microsaccades and drift to preventing fading in human vision. Our results indicate that both microsaccades and drift mediate the prevention of visual fading. We also found that drift is a potentially larger contributor to preventing fading than microsaccades, although microsaccades are more effective than drift. Microsaccades moreover prevented foveal and peripheral fading in an equivalent fashion, and their efficacy was independent of their size, number, and direction. Our data also suggest that faster drift may prevent fading better than slower drift. These findings may help to reconcile the long-standing controversy concerning the comparative roles of microsaccades and drift in visibility during fixation.

Saccades are rapid eye movements that change the line of sight between successive points of fixation. Even as we attempt to fixate our gaze precisely, small rapid eye movements called microsaccades interrupt fixation one or two times each second. Although the neural pathway controlling saccade generation is well understood, the specific mechanism for triggering microsaccades is unknown. Here, we review the evidence suggesting that microsaccades and saccades are generated by the same neural pathway. We also discuss current models of how the saccadic system produces microsaccades. Finally, we propose a new mechanism for triggering both microsaccades and saccades, based on a circuit formed by omnipause and long-lead burst neurons and driven by activity in the superior colliculus. Our model differs from previous proposals in that it does not require superior colliculus activity to surpass a particular threshold to trigger microsaccades and saccades. Rather, we propose that the reciprocal inhibition between omnipause and long-lead burst neurons gates each microsaccadic or saccadic event, triggering the eye movement whenever the activity in the long-lead burst neurons overcomes the inhibition from the omnipause neurons.

[Abstract] We have tested the effect of iontophoretic application of the nitric oxide synthase inhibitor l-nitroarginine on the activity of a population of 53 perigeniculate (PGN) cells, recorded extracellularly in the anaesthetized paralysed cat. In all cells tested with visual stimulation during l-nitroarginine application (n= 15), the visually elicited responses were markedly reduced, on average by 63 ± 15%, and there was a reduction in spontaneous activity too. This effect was blocked by co-application of the substrate for nitric oxide synthase, l-arginine, but not by the inactive d-isoform, although application of l-arginine alone was without effect. Pressure application of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) elevated both visual responses and spontaneous discharge, an effect also seen with a second nitric oxide donor, sodium nitroprusside (n= 12). The nitric oxide synthase inhibitor l-nitroarginine was applied to a sub-population of seven cells and it selectively decreased NMDA mediated excitation (reduction 80 % 14%) with little or no effect on the excitation mediated by α-amino-3-hydroxy-5-5-methyl-4-isoxazole-propionic acid (AMPA) or quisqualate (effects not statistically significant), and it had no effect (n= 7) on excitation mediated by the metabotropic agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD). Furthermore, application of SNAP also increased the magnitude of excitatory responses mediated by NMDA receptors. On a different population of seven cells, application of the new NO donor diethylamine-nitric oxide (DEA-NO) enhanced the actions Of NMDA without an effect on responses to AMPA. These effects are qualitatively and quantitatively similar to those we have previously described for X and Y type cells in the dorsal lateral geniculate nucleus (dLGN), despite the known opposite effects of acetylcholine (ACh) application in the dLGN and PGN (ACh is co-localized with nitric oxide synthase at both sites). We propose that within the PGN nitric oxide acts to enhance transmission utilizing NMDA receptors selectively (thereby interacting with the globally inhibiting effect of ACh at this site) to enhance visual responses, reducing or removing the non-specific inhibitory drive from PGN to dLGN seen in the spindling activity of slow-wave sleep. These effects will act in concert with the facilitatory actions of both ACh and nitric oxide within the dLGN proper, and will thereby enhance the faithful transmission of visual information from retina to cortex. Ministerio de Educación y Ciencia; PB93-0347

[Abstract] We have examined the responses of a population of 77 cells in the dorsal lateral geniculate nucleus (dLGN) of the anaesthetized, paralysed cat. Here the synthetic enzyme for the production of nitric oxide, nitric oxide synthase, is found only in the presynaptic terminals of the cholinergic input from the brainstem. In our hands, iontophoretic application of inhibitors of this enzyme resulted both in significant decreases in visual responses and decreased responses to exogenous application of NMDA, effects which were reversed by coapplication of the natural substrate for nitric oxide synthase, L-arginine, but not the biologically inactive isomer, D-arginine. Nitroprusside and S-nitroso-N-acetylpenicillamine (SNAP), nitric oxide donors, but not L-arginine, were able to increase markedly both spontaneous activity and the responsiveness to NMDA application. Furthermore, SNAP application facilitated visual responses. Responses of cells in animals without retinal, cortical and parabrachial input to the LGN suggest a postsynaptic site of action of nitric oxide. This modulation of the gain of visual signals transmitted to the cortex suggests a completely novel pathway for nitric oxide regulation of function, as yet described only in primary sensory thalamus of the mammalian central nervous system. Ministerio de Educación y Ciencia; PB93-0347