Y. Howard Li

All Publications

• Chromatic induction and retinal image motion. Perception Li, Y. H., Rucci, M., Aguado, B., Maho, C. M., Poletti, M., Brenner, E. 2026: 3010066251409616

  Abstract

  As the eyes drift across a scene, borders between surfaces slide across the retina. Consequently, near borders' edges, parts of the retina that have adapted to the light at one side of the border are exposed to the light at the other side of the border. Such changes in exposure might increase the judged contrast. Retinal image motion might therefore contribute to chromatic induction, the influence that adjacent colours have on a surface's apparent colour, by increasing the apparent colour contrast. We conducted two experiments to evaluate this possibility. The experiments examined how artificially increasing or decreasing the extent to which certain surface borders shift across the retina influences the perceived colour. Neither increasing nor decreasing the extent to which selected borders shift across the retina had a substantial influence on the perceived colour. This implies that chromatic induction does not arise from overestimating the contrast between adjacent surfaces when small eye movements shift the border between those surfaces across the retina.

  View details for DOI 10.1177/03010066251409616

  View details for PubMedID 41499284

• Consequences of eye movements for spatial selectivity. Current biology : CB Intoy, J., Li, Y. H., Bowers, N. R., Victor, J. D., Poletti, M., Rucci, M. 2024; 34 (14): 3265-3272.e4

  Abstract

  What determines spatial tuning in the visual system? Standard views rely on the assumption that spatial information is directly inherited from the relative position of photoreceptors and shaped by neuronal connectivity.1,2 However, human eyes are always in motion during fixation,3,4,5,6 so retinal neurons receive temporal modulations that depend on the interaction of the spatial structure of the stimulus with eye movements. It has long been hypothesized that these modulations might contribute to spatial encoding,7,8,9,10,11,12 a proposal supported by several recent observations.13,14,15,16 A fundamental, yet untested, consequence of this encoding strategy is that spatial tuning is not hard-wired in the visual system but critically depends on how the fixational motion of the eye shapes the temporal structure of the signals impinging onto the retina. Here we used high-resolution techniques for eye-tracking17 and gaze-contingent display control18 to quantitatively test this distinctive prediction. We examined how contrast sensitivity, a hallmark of spatial vision, is influenced by fixational motion, both during normal active fixation and when the spatiotemporal stimulus on the retina is altered to mimic changes in fixational control. We showed that visual sensitivity closely follows the strength of the luminance modulations delivered within a narrow temporal bandwidth, so changes in fixational motion have opposite visual effects at low and high spatial frequencies. By identifying a key role for oculomotor activity in spatial selectivity, these findings have important implications for the perceptual consequences of abnormal eye movements, the sources of perceptual variability, and the function of oculomotor control.

  View details for DOI 10.1016/j.cub.2024.06.016

  View details for PubMedID 38981478

  View details for PubMedCentralID PMC11348862

• Fine-scale measurement of the blind spot borders. Vision research Meermeier, A., Lappe, M., Li, Y. H., Rifai, K., Wahl, S., Rucci, M. 2023; 211: 108208

  Abstract

  The blind spot is both a necessity and a nuisance for seeing. It is the portion of the visual field projecting to where the optic nerve crosses the retina, a region devoid of photoreceptors and hence visual input. The precise way in which vision transitions into blindness at the blind spot border is to date unknown. A chief challenge to map this transition is the incessant movement of the eye, which unavoidably smears measurements across space. In this study, we used high-resolution eye-tracking and state-of-the-art retinal stabilization to finely map the blind spot borders. Participants reported the onset of tiny high-contrast probes that were briefly flashed at precise positions around the blind spot. This method has sufficient resolution to enable mapping of blood vessels from psychophysical measurements. Our data show that, even after accounting for eye movements, the transition zones at the edges of the blind spot are considerable. On the horizontal meridian, the regions with detection rates between 80% and 20% span approximately 25% of the overall width of the blind spot. These borders also vary considerably in size across different axes. These data show that the transition from full visibility to blindness at the blind spot border is not abrupt but occurs over a broad area.

  View details for DOI 10.1016/j.visres.2023.108208

  View details for PubMedID 37454560

  View details for PubMedCentralID PMC10494866

• Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis. Brain, behavior, and immunity Hammond, J. W., Bellizzi, M. J., Ware, C., Qiu, W. Q., Saminathan, P., Li, H., Luo, S., Ma, S. A., Li, Y., Gelbard, H. A. 2020; 87: 739-750

  Abstract

  Multiple sclerosis (MS) is an inflammatory, neurodegenerative disease of the CNS characterized by both grey and white matter injury. Microglial activation and a reduction in synaptic density are key features of grey matter pathology that can be modeled with MOG35-55 experimental autoimmune encephalomyelitis (EAE). Complement deposition combined with microglial engulfment has been shown during normal development and in disease as a mechanism for pruning synapses. We tested whether there is excess complement production in the EAE hippocampus and whether complement-dependent synapse loss is a source of degeneration in EAE using C1qa and C3 knockout mice. We found that C1q and C3 protein and mRNA levels were elevated in EAE mice. Genetic loss of C3 protected mice from EAE-induced synapse loss, reduced microglial activation, decreased the severity of the EAE clinical score, and protected memory/freezing behavior after contextual fear conditioning. C1qa KO mice with EAE showed little to no change on these measurements compared to WT EAE mice. Thus, pathologic expression and activation of the early complement pathway, specifically at the level of C3, contributes to hippocampal grey matter pathology in the EAE.

  View details for DOI 10.1016/j.bbi.2020.03.004

  View details for PubMedID 32151684

  View details for PubMedCentralID PMC8698220