Although visual discomfort symptoms associated with near work have been correlated with clinical measures of accommodation, studies using objective recordings have not found corresponding deficits in accommodative function. One problem with previous studies is that accommodation measures have been too brief to assess accommodative fatigue. This study examined steady state accommodative responses among a college population with visual discomfort, over a 90-s time period. Thirty-one participants were grouped into high (n = 15) or low visual discomfort groups (n = 16) based on their scores on the Conlon Visual Discomfort Survey. Using the WAM-5500 autorefractor, accommodation responses were recorded at 5 Hz for two consecutive minutes at five viewing distances. The results showed a significant interaction between the high and low discomfort groups over time in accommodation response. The high discomfort group showed an increase in accommodative lag, whereas the low discomfort group had a stable response. Our study suggests that the high visual discomfort group is characterized by accommodative fatigue, with a higher lag of accommodation developing at a near viewing distance over time.

Previous studies have identified a magnocellular pathway defect in approximately 75% of dyslexics. Since these experiments have not classified dyslexia into subtypes, the purpose of this experiment was to determine if adult dyseidetic dyslexics or dysphoneidetic dyslexics suffer from a defect in the magnocellular pathway. Nine dyseidetic dyslexics, eight dysphoneidetic dyslexics, and nine normal readers participated in the experiment. Contrast sensitivity functions (CSF) were determined with vertically oriented sine wave gratings (0.5, 1.0, 2.0, 4.0, 8.0, 12.0 c/deg drifting at 1 and 10 Hz) by employing a two-alternative, forced-choice technique. The results of the experiment indicated that dysphoneidetic dyslexics had reduced sensitivity to low spatial frequencies at 10 Hz, whereas dyseidetic dyslexics did not have reduced sensitivity at either 1 or 10 Hz. These results suggest that the type of dyslexia influences whether losses in perception are found which are consistent with a magnocellular deficit.

The visual evoked potential (VEP) in the mouse is characterized and compared to responses obtained with the electroretinogram (ERG). The results indicate that: 1, the VEP originates in the visual cortex; 2, the rod and cone pathways contribute separately to the VEP; 3, temporal tuning functions for rod and cone ERGs are low pass and band pass, respectively; VEP tuning functions are both band pass; and 4, VEP acuity is 0.62+/-0.156 cycles/degree. The differences in the spatial and temporal tuning functions obtained from the retina and visual cortex provides a tool to investigate signal processing through the visual system.

The purpose of this investigation was to analyze the influence of stimulus orientation on the responses of individual neurons in the monkey's lateral geniculate nucleus (LGN). Our specific goals were to assess the prevalence and the degree of orientation tuning in the monkey LGN and to determine if the preferred stimulus orientations of LGN neurons varied as a function of receptive-field position. The primary motivation for this research was to gain insight into the receptive-field configuration of LGN neurons and consequently into the neural mechanisms which determine the spatial organization of LGN receptive fields in primates.In both the parvocellular and magnocellular layers, the responses of the majority of individual neurons to sine-wave gratings varied as a function of stimulus orientation. The influence of stimulus orientation was, however, highly dependent on the spatial characteristics of the stimulus; the greatest degree of orientation bias was observed for spatial frequencies higher than the cell's optimal spatial frequency. On a population basis, the degree of orientation bias was similar for all major classes of LGN neurons (e.g. ON vs. OFF center; parvocellular vs. magnocellular) and did not vary systematically with receptive-field eccentricity. At a given receptive-field location, LGN neurons, particularly cells in the parvocellular laminae, tended to prefer either radially oriented stimuli or stimuli oriented more horizontally than their polar axis. Our analyses of the orientation-dependent changes in spatial-frequency response functions, which was based on the Soodak et al., (1987; Soodak, 1986) two-dimensional, difference-of-Gaussian receptive-field model, suggested that the orientation bias in LGN neurons was due to an elongation of the receptive-field center mechanism which in some cases appeared to consist of multiple subunits. Direct comparisons of the orientation-tuning characteristics of LGN cells and their retinal inputs (S potentials) indicated that the orientation bias in the monkey LGN reflects primarily the functional properties of individual retinal ganglion cells. We conclude that orientation sensitivity is a significant property of subcortical neurons in the primate's geniculo-cortical pathway.

Axon injury is an early event in neurodegenerative diseases that often leads to retrograde neuronal cell death and progressive permanent loss of vital neuronal functions. The connection of these two obviously sequential degenerative events, however, is elusive. Deciphering the upstream signals that trigger the neurodegeneration cascades in both neuronal soma and axon would be a key step toward developing the effective neuroprotectants that are greatly needed in the clinic. We showed previously that optic nerve injury-induced neuronal endoplasmic reticulum (ER) stress plays an important role in retinal ganglion cell (RGC) death. Using two in vivo mouse models of optic neuropathies (traumatic optic nerve injury and glaucoma) and adeno-associated virus-mediated RGC-specific gene targeting, we now show that differential manipulation of unfolded protein response pathways in opposite directions-inhibition of eukaryotic translation initiation factor 2␣-C/EBP homologous protein and activation of X-box binding protein 1-promotes both RGC axons and somata survival and preserves visual function. Our results indicate that axon injury-induced neuronal ER stress plays an important role in both axon degeneration and neuron soma death. Neuronal ER stress is therefore a promising therapeutic target for glaucoma and potentially other types of neurodegeneration.