SUMMARY1. A method ofproducing red-green and blue-yellow sinusoidal chromatic gratings is used which permits the correction of all chromatic aberrations.2. A quantitative criterion is adopted to choose the intensity match of the two colours in the stimulus: this is the intensity ratio at which contrast sensitivity for the chromatic grating differs most from the contrast sensitivity for a monochromatic luminance grating. Results show that this intensity match varies with spatial frequency and does not necessarily correspond to a luminance match between the colours.3. Contrast sensitivities to the chromatic gratings at the criterion intensity match are measured as a function of spatial frequency, using field sizes ranging from 2 to 23 deg. Both blue-yellow and red-green contrast sensitivity functions have similar low-pass characteristics, with no low-frequency attenuation even at low frequencies below 041 cycles/deg. These functions indicate that the limiting acuities based on red-green and blue-yellow colour discriminations are similar at 11 or 12 cycles/deg.4. Comparisons between contrast sensitivity functions for the chromatic and monochromatic gratings are made at the same mean luminances. Results show that, at low spatial frequencies below 0 5 cycles/deg, contrast sensitivity is greater to the chromatic gratings, consisting of two monochromatic gratings added in antiphase, than to either monochromatic grating alone. Above 0-5 cycles/deg, contrast sensitivity is greater to monochromatic than to chromatic gratings.

SUMMARY1. The aim of this study was to determine whether optical, receptoral or higherorder neural properties limit spatial resolution (acuity) in human vision, especially in the peripheral regions of the visual field.2. Both achromatic and chromatic stimuli were used, and measures were taken to ensure that the resolution estimates were not contaminated by the detection of spatial sampling artifacts. Spatial contrast sensitivity functions were measured at retinal locations from 0 to 55 deg along the naso-temporal meridian for: (i) discriminating the direction of drift of luminance-modulated (black-white) sinusoidal stimuli drifting at 8 Hz (achromatic task); and (ii) for detecting isoluminant red-green sinusoidal stimuli drifting at 0-4 Hz (chromatic task). Achromatic contrast sensitivity functions were also measured along the vertical meridian for eccentricities of 8 and 40 deg. Each achromatic function was extrapolated to a contrast sensitivity of one (100 % contrast) to estimate achromatic acuity. Chromatic acuities were obtained by expressing chromatic contrast in terms of cone contrasts and using the same method of extrapolation. We compared the results with recent data on human optical properties and retinal anatomy.3. Both achromatic and chromatic acuity decline with distance from the fovea, but at a faster rate than that dictated by the known optical and/or receptoral properties of the human eye. We conclude that, for stimuli -of either achromatic or chromatic contrast, peripheral spatial resolution is limited by post-receptoral mechanisms. Also, chromatic acuity declines more steeply than luminance acuity with eccentricity suggesting that there are additional post-receptoral limitations on colour resolution in the periphery.4. A clear naso-temporal asymmetry is seen in the resolution whose dependence is qualitatively, but not quantitatively, similar to the Nyquist limits imposed by the asymmetric density of human retinal ganglion cells. We discuss the possibility that

Our aim was to make a quantitative comparison of the response of the different visual cortical areas to selective stimulation of the two different cone-opponent pathways [long- and medium-wavelength (L/M)- and short-wavelength (S)-cone-opponent] and the achromatic pathway under equivalent conditions. The appropriate stimulus-contrast metric for the comparison of colour and achromatic sensitivity is unknown, however, and so a secondary aim was to investigate whether equivalent fMRI responses of each cortical area are predicted by stimulus contrast matched in multiples of detection threshold that approximately equates for visibility, or direct (cone) contrast matches in which psychophysical sensitivity is uncorrected. We found that the fMRI response across the two colour and achromatic pathways is not well predicted by threshold-scaled stimuli (perceptual visibility) but is better predicted by cone contrast, particularly for area V1. Our results show that the early visual areas (V1, V2, V3, VP and hV4) all have robust responses to colour. No area showed an overall colour preference, however, until anterior to V4 where we found a ventral occipital region that has a significant preference for chromatic stimuli, indicating a functional distinction from earlier areas. We found that all of these areas have a surprisingly strong response to S-cone stimuli, at least as great as the L/M response, suggesting a relative enhancement of the S-cone cortical signal. We also identified two areas (V3A and hMT+) with a significant preference for achromatic over chromatic stimuli, indicating a functional grouping into a dorsal pathway with a strong magnocellular input.

The color vision of Old World primates and humans uses two cone-opponent systems; one differences the outputs of L and M cones forming a red-green (RG) system, and the other differences S cones with a combination of L and M cones forming a blue-yellow (BY) system. In this paper, we show that in human vision these two systems have a differential distribution across the visual field. Cone contrast sensitivities for sine-wave grating stimuli (smoothly enveloped in space and time) were measured for the two color systems (RG & BY) and the achromatic (Ach) system at a range of eccentricities in the nasal field (0-25 deg). We spatially scaled our stimuli independently for each system (RG, BY, & Ach) in order to activate that system optimally at each eccentricity. This controlled for any differential variations in spatial scale with eccentricity and provided a comparison between the three systems under equivalent conditions. We find that while red-green cone opponency has a steep decline away from the fovea, the loss in blue-yellow cone opponency is more gradual, showing a similar loss to that found for achromatic vision. Thus only red-green opponency, and not blue-yellow opponency, can be considered a foveal specialization of primate vision with an overrepresentation at the fovea. In addition, statistical calculations of the level of chance cone opponency in the two systems indicate that selective S cone connections to postreceptoral neurons are essential to maintain peripheral blue-yellow sensitivity in human vision. In the red-green system, an assumption of cone selectivity is not required to account for losses in peripheral sensitivity. Overall, these results provide behavioral evidence for functionally distinct neuro-architectural origins of the two color systems in human vision, supporting recent physiological results in primates.

Amblyopia or lazy eye is the most common cause of uniocular blindness in adults. It is caused by a disruption to normal visual development as a consequence of unmatched inputs from the two eyes in early life, arising from a turned eye (strabismus), unequal refractive error (anisometropia) or form deprivation (e.g. cataract). Animal models based on extracellular recordings in anesthetized animals suggest that the earliest site of the anomaly in the primate visual pathway is the primary visual cortex (corresponding to the striate cortex, cytoarchitectonic area 17 and area V1), which is where inputs from the two eyes are first combined in an excitatory fashion, whereas more distal and monocular processing structures such as the retina and lateral geniculate nucleus (LGN) are normal. Using high-field functional magnetic resonance imaging in a group of human adults with amblyopia, we demonstrate that functional deficits are first observable at a thalamic level, that of the LGN. Our results suggest the need to re-evaluate the current models of amblyopia that are based on the assumption of a purely cortical dysfunction, as well as the role for the LGN in visual development.

No abstract

Fragile X syndrome (FXS) is the most common form of heritable mental retardation, affecting approximately 1 in 4000 males. The syndrome arises from expansion of a trinucleotide repeat in the 5'-untranslated region of the fragile X mental retardation 1 (FMR1) gene, leading to methylation of the promoter sequence and lack of the fragile X mental retardation protein (FMRP). Affected individuals display a unique neurobehavioural phenotype that includes striking visual-motor deficits. Here we provide neurobiological and behavioural evidence that supports the hypothesis that these visual-motor deficits are attributable to a magnocellular (M) visual pathway impairment. Immunohistochemical staining of a lateral geniculate nucleus (LGN) of a normal human male revealed high FMRP basal expression selectively within the M layers, suggesting an increased susceptibility of these neurons to the lack of FMRP as occurs in FXS. Similar staining of monkey LGNs for quantification purposes revealed that the difference is not an artefact of cell size differences between M and parvocellular (P) neurons. Further, Nissl staining of the LGNs of a male FXS patient revealed alaminar nuclei comprised of a homogenous population of small sized neurons, providing anatomical and morphological support for the idea that an M pathway pathology exists in FXS. Consistent with these neurobiological data, we have found that male patients with FXS have reduced sensitivity for psychophysical stimuli that probe the M pathway but not for those that probe the P pathway, a complementary visual stream that performs a separate set of early visual operations. Finally, male patients with FXS performed poorly on a global motion task but not on a form perception task, suggesting that the M pathway thalamic deficit may have a selective impact on cortical visual functioning in the parietal lobe, which is known to be a major recipient of M pathway afferents via the primary visual cortex. Together, these findings provide the first evidence that the loss of a single gene product, FMRP, in humans leads to abnormal neuroanatomical morphology of the LGN and a concomitant selective visual deficit of the M pathway.

On the basis of the early primate neurophysiological recordings, it was thought that the different cone types of the primate retina project selectively into the centre and surround of the receptive fields of cone opponent neurons, and more recently this view has been reasserted on the basis of physiological results. An alternative idea is that these projections are in fact unselective for cone type, and, therefore, cone opponency arises from chance variations in the proportions of different cone types in centre and surround. The issue is presently controversial with anatomical or physiological support for both hypotheses. Our results show that there is a selective loss of red-green colour sensitivity across the human visual field. Furthermore, this selective loss occurs under low temporal frequency conditions (0.5 Hz) which were selected to favour the mediation of both colour and luminance detection by a common P cell pathway and to exclude an M cell contribution to detection threshold. We show that "hit and miss" post-receptoral cone projections will produce a decline in cone opponency that is sufficient to account for this selective loss, thus providing psychophysical evidence consistent with this hypothesis.