Neuroglobin - a potential biological marker of retinal damage induced by LED light.

Neuroglobin (NGB), a protein highly expressed in the retina, has been shown to be up-regulated to protect neurons from hypoxic and ischemic injuries. It exhibits neuroprotective functions and plays an important role in the survival of neurons. Recent studies show that light-emitting diode (LED) white light emitted significant amounts of blue light (short-wavelength), which may be harmful to retinal cells, but the studies about biomarkers for evaluating the damage from LED white light are still insufficient. In our study, we found that NGB levels in the retina showed a twofold increase and peaked at 1h after a 1-h exposure to blue light (453 nm) which did not cause damage to the retina. However, retinal damage was observed after 2h of blue-light irradiation, which induced an approximate sevenfold increase of NGB levels as confirmed by Western blot and RT-PCR analysis. Immunofluorescence study demonstrated that NGB was predominantly up-regulated in the ganglion cell layer (GCL), plexiform layer (PL) and photoreceptor layer (PRL). We also examined Ngb mRNA and protein expression in the damaged retina induced by light of other wavelengths given equal photon fluxes. The LED red light (625 nm), green light (527 nm) and blue light (453 nm) increased the expression of NGB and caused TdT-mediated dUTP nick-end labeling-positive cells, especially in the blue-light group. In addition, a negative correlation between NGB and rhodopsin was observed. These findings suggested that there was a correlation between NGB expression and the severity of the retinal damage, indicating NGB's potential function as a biological marker of retinal damage induced by LED light.

Vestibular signals can distort the perceived spatial relationship of retinal stimuli.

The flash-lag phenomenon is an illusion that affects the perceived relationship of a moving object and a briefly visible one: the moving object appears to be ahead of the flashed one. In practically all studies of this phenomenon, the image of the object moves on the retina as the object moves in space. Therefore, explanations of the illusion were sought in terms of purely visual mechanisms. Here we set up a situation in which the object's motion in space is entirely produced by passive rotation of the subject. No motion occurred on the retina. The visual display (a continuously lit stimulus and a flashed one) was mounted on a vestibular chair. While the subjects fixated this display, they were rotated in the dark at a constant speed and suddenly stopped. Perceptual misalignment (flash-lag) was robust and consistent during both the initial phase of rotation and the postrotary period when neither chair, subject, nor stimulus was actually moving. As a vestibular signal can cause an illusory spatial dissociation in the visual domain, we conclude that the mechanism of the flash-lag must be more general than was thought up-to-now.

Perceived geometrical relationships affected by eye-movement signals.

To determine the location of visual objects relative to the observer, the visual system must take account not only of the location of the stimulus on the retina, but also of the direction of gaze. In contrast, the perceived spatial relationship between visual stimuli is normally assumed to depend on retinal information alone, and not to require information about eye position. We now show, however, that the perceived alignment of three dots-tested by a vernier alignment task-is systematically altered in the period immediately preceding a saccade. Thus, information about eye position can modify not only the perceived relationship of the entire retinal image to the observer, but also the relations between elements within the image. The processing of relative position and of egocentric (observer-centred) position may therefore be less distinct than previously believed.