The current study tested the development of face and object processing in young children (mean age = 5.24 years), adolescents (mean age = 15.8 years), and adults (mean age = 21.1 years) using stimuli that were equated for low-level visual characteristics (luminance, contrast, and spatial frequency make-up) and methods that equate for difficulty across ages. We also tested sensitivity to luminance and chromatic contrast (i.e., thought to be mediated primarily by the subcortical Magnocellular (M) and Parvocellular (P) pathways, respectively) to determine whether age-related improvements in face or object discrimination were driven by age-related changes in the M and/or P pathways. Results showed a selective age-related improvement in face sensitivity and a relationship between age-related increases in face sensitivity and luminance contrast sensitivity. These results add to the mounting evidence that the M pathway may influence face processing.

The aim was to investigate the temporal response properties of magnocellular, parvocellular, and koniocellular visual pathways using increment/decrement changes in contrast to elicit visual evoked potentials (VEPs). Static achromatic and isoluminant chromatic gratings were generated on a monitor. Chromatic gratings were modulated along red/green (R/G) or subject-specific tritanopic confusion axes, established using a minimum distinct border criterion. Isoluminance was determined using minimum flicker photometry. Achromatic and chromatic VEPs were recorded to contrast increments and decrements of 0.1 or 0.2 superimposed on the static gratings (masking contrast 0–0.6). Achromatic increment/decrement changes in contrast evoked a percept of apparent motion when the spatial frequency was low; VEPs to such stimuli were positive in polarity and largely unaffected by high levels of static contrast, consistent with transient response mechanisms. VEPs to finer achromatic gratings showed marked attenuation as static contrast was increased. Chromatic VEPs to R/G or tritan chromatic contrast increments were of negative polarity and showed progressive attenuation as static contrast was increased, in keeping with increasing desensitization of the sustained responses of the color-opponent visual pathways. Chromatic contrast decrement VEPs were of positive polarity and less sensitive to pattern adaptation. The relative contribution of sustained/transient mechanisms to achromatic processing is spatial frequency dependent. Chromatic contrast increment VEPs reflect the sustained temporal response properties of parvocellular and koniocellular pathways. Cortical VEPs can provide an objective measure of pattern adaptation and can be used to probe the temporal response characteristics of different visual pathways.

If the relative phase of red and green modulated lights is changed, at low temporal frequencies the response of cells of the magnocellular (MC) pathway has been found to be minimal not to counterphase, chromatic modulation (as expected of a luminance mechanism) but shifted to some phase intermediate between luminance and chromatic modulation. The results could only be modeled by assuming interaction between achromatic and chromatic inputs to MC cells. The ‘phase shift’ resembled that seen with psychophysical threshold measurements using the same stimuli. Psychophysical results also showed that the phase shift is dependent on the chromaticity of a background. The results reported here show that the direction of the phase shift in MC cells is reversed by changing the background from long to short wavelengths and is consistent with psychophysical observations. Cell behavior was again modeled by assuming vector summation of achromatic and chromatic inputs. The reversal of phase-shift direction requires a reversal in polarity of the chromatic input. The underlying physiological mechanism may involve summation of chromatic signals of opposite polarity; if the relative size of these signals depends on the background, this may determine the direction of phase shift.

Visually evoked field potentials in human subjects and single-cell responses from retinal ganglion cells in the macaque monkey were compared in closely similar stimulus situations. The classical heterochromatic flicker photometry (HFP) technique was used to measure spectral sensitivity in man, both psychophysically and by recording the 40-Hz response, and to measure the spectral sensitivity of magnocellular (MC-) pathway cells of the macaque. The three measures gave closely similar spectral-sensitivity curves. Close agreement between the three measures was also found when the variable-modulation HFP technique was used to measure spectral sensitivity. When the relative phase between red and green lights was varied, the point of minimum subjective flicker for human observers was close to a sharp minimum found in the amplitude of the 40-Hz response in human and was also close to a minimum in the response of MC-pathway neurons in the monkey. The human 40-Hz response saturated at between 10 and 30% modulation depth, and so did the response of MC-pathway cells in the monkey.

The 16-Hz response in human showed none of the above correlations with MC-pathway properties. On the other hand, parvocellular (PC-) pathway cells responded vigorously to constant-luminance, chromatic modulation, at frequencies higher than can be detected by human observers. The human 16-Hz response also was strong in that stimulus situation. In addition, the response of PC-pathway cells on increasing modulation depth showed little saturation, and this behaviour was paralleled by the human 16-Hz response.

We conclude that the properties of MC-pathway neurons in macaque are closely similar to the properties of the human 40-Hz response in the respects just described. We suggest that the 40-Hz response may offer a means of objectively isolating and investigating the contribution of the magnocellular stream to cortical activity in human. In contrast, the properties of PC-pathway neurons in macaque are quite different from the properties of the human 40-Hz response, and in several respects resemble the properties of the human 16-Hz response.

Visual localization was studied by flashing small stimuli on a green background and requiring observers to press keys to indicate whether the stimulus appeared to the left or right of fixation. The results suggest that, for small (0.25 deg) briefly flashed (17 ms) stimuli at an eccentric location (10 deg), color contrast is not useable and localization presumably must rely on the magnocellular pathway. When stimulus size and duration were increased at 10-deg eccentricity, isochromatic stimuli could be localized at less than 10% luminance contrast (again suggesting use of the magnocellular high sensitivity luminance-contrast system), but isoluminant color-contrast stimuli could also be localized (suggesting use of the color-contrast sensitive parvocellular system). Thus, the results indicate that, dependent on stimulus conditions, both magnocellular and parvocellular pathways were utilized by normal observers in this localization task.

Ibotenic-acid lesions of the magnocelluar portion of the macaque lateral geniculate nucleus were used to examine the role of the M-cell pathway in spatio-temporal contrast sensitivity. A lesion was place in layer 1 of the lateral geniculate of each of two monkeys. Physiological mapping in one animal demonstrated that the visual-field locus of the lesion was on the horizontal meridian, approximately 6 deg in the temporal field. Visual thresholds were tested monocularly in the contralateral eye, and fixation locus was monitored with a scleral search coil to control the retinal location of the test target.

Three threshold measures were clearly disrupted by the magnocellular lesions. Contrast sensitivity for a 1 cycle/deg grating that drifted at 10 Hz was reduced from about twofold greater than, to about the same as, that for 10-Hz counterphase modulated gratings. Sensitivity for a very low spatial frequency (Gaussian blob), 10-Hz flickering stimulus was reduced so severely that no threshold could be measured. In addition, flicker resolution was greatly reduced at lower modulation depths (0.22), but not at higher depths (1.0). Two of the measured thresholds were unaffected by the lesions. Contrast sensitivity for 2 cycle/deg stationary gratings remained intact, and little or no effect on sensitivity was found for 1 cycle/deg, 10-Hz counterphase modulated gratings.

Together, these results suggest that the magnocellular pathway makes little contribution to visual sensitivity at low to moderate temporal frequencies. On the other hand, some contribution to detection sensitivity is evident at lower spatial and high temporal frequencies, especially for drifting stimuli. It appears that a major role of the magnocellular pathway may be to provide input to cortical mechanisms sensitive to rapid visual motion.

Latencies to small flashing spots of light were measured in different layers of areas V1 and V2 in anesthetized and paralyzed macaque monkeys. The shortest latencies were found in layers 4Cα and 4B of area V1. Latencies in layer 4Cβ were on average 20 ms longer than those in 4Cα and 4B. The shortest latencies in area V2 were observed in the infragranular layers and they did not differ significantly from those found in the infragranular layers in V1. Similarly, latencies in the supragranular layers of V2 were not significantly different from those measured in the supragranular layers of V1. These results show that, in area V1, neurons of the magnocellular pathway are activated on average 20 ms earlier than those of the parvocellular pathway. Our data also suggest that much processing begins simultaneously in areas V1 and V2.

Five lagged cells were recognized by extracellular recording in the lateral geniculate nucleus of an awake, behaving macaque monkey. Previous reports of lagged cells were all in the anesthetized cat. Both parvocellular and magnocellular lagged cells were observed. Response timing was distributed continuously across the population, and both sustained and transient responses were seen in the magnocellular subpopulation. Cortex thus receives signals with a wide range of timing, which can mediate direction selectivity across multiple dimensions.

We examined achromatic contrast discrimination in asymptomatic carriers of 11778 Leber‘s hereditary optic neuropathy (LHON 18 controls) and 18 age-match were also tested. To evaluate magnocellular (MC) and Parvocellular (PC) contrast discrimination, we used a version of Pokorny and Smith's (1997) pulsed/steady-pedestal paradigms (PPP/SPP) thought to be detected via PC and MC pathways, respectively. A luminance pedestal (four 1° × 1° squares) was presented on a 12 cd/m2 surround. The luminance of one of the squares (trial square, TS) was randomly incremented for either 17 or 133 ms. Observers had to detect the TS, in a forced-choice task, at each duration, for three pedestal levels: 7, 12, 19 cd/m2. In the SPP, the pedestal was fixed, and the TS was modulated. For the PPP, all four pedestal squares pulsed for 17 or 133 ms, and the TS was simultaneously incremented or decremented. We found that contrast discrimination thresholds of LHON carriers were significantly higher than controls' in the condition with the highest luminance of both paradigms, implying impaired contrast processing with no evidence of differential sensitivity losses between the two systems. Carriers’ thresholds manifested significantly longer temporal integration than controls in the SPP, consistent with slowed MC responses. The SPP and PPP paradigms can identify contrast and temporal processing deficits in asymptomatic LHON carriers, and thus provide an additional tool for early detection and characterization of the disease.

Luminance signals mediated by the magnocellular (MC) pathway play an important role in vernier tasks. MC ganglion cells show a phase advance in their responses to sinusoidal stimuli with increasing contrast due to contrast gain control mechanisms. If the phase information in MC ganglion cell responses were utilized by central mechanisms in vernier tasks, one might expect systematic errors caused by the phase advance. This systematic error may contribute to the contrast paradox phenomenon, where vernier performance deteriorates, rather than improves, when only one of the target pair increases in contrast. Vernier psychometric functions for a pair of gratings of mismatched contrast were measured to seek such misestimation. In associated electrophysiological experiments, MC and parvocellular (PC) ganglion cells' responses to similar stimuli were measured to provide a physiological reference. The psychophysical experiments show that a high-contrast grating is perceived as phase advanced in the drift direction compared to a low-contrast grating, especially at a high drift rate (8 Hz). The size of the phase advance was comparable to that seen in MC cells under similar stimulus conditions. These results are consistent with the MC pathway supporting vernier performance with achromatic gratings. The shifts in vernier psychometric functions were negligible for pairs of chromatic gratings under the conditions tested here, consistent with the lack of phase advance both in responses of PC ganglion cells and in frequency-doubled chromatic responses of MC ganglion cells.

Neural models of retinal processing provide an important tool for analyzing retinal signals and their functional significance. However, it is here argued that in biological reality, retinal connectivity is unlikely to be as specific as ideal neural models might suggest. The retina is thought to provide functionally specific signals, but this specificity is unlikely to be anatomically complete. This is illustrated by examples of cone connectivity to macaque ganglion cells. For example, cells of the magnocellular pathway appear to avoid short-wavelength cone input, so that such input is negligible under normal conditions. However, there is anatomical, physiological, and psychophysical evidence that under special conditions, weak input may be revealed. Second, ideal models of how retinal information is centrally utilized have to take into account the biological reality of retinal signals. The stochastic nature of impulse trains modifies signal-to-noise ratio in unexpected ways. Also, non-linearities in cell responses make, for example, multiplexing of luminance and chromatic signals in the parvocellular pathway impracticable. The purpose of this analysis is to show than ideal neural models must confront an often more complex and nuanced physiological reality.

In metacontrast a masking stimulus reduces the visibility of an adjacent target stimulus. This effect has been interpreted in terms of magno-/parvocellular interactions. It has also been found that a second masking stimulus, which precedes the primary mask by about 90 ms reduces the masking effect. This reduction, which is termed “target recovery,” has been hypothesized to reflect parvocellular inhibition of the magnocellular system. However, this is problematic because the time course of this effect is much larger than would be expected from magno-/parvocellular interactions. For this and other reasons, it is difficult to understand metacontrast in terms of magno- and parvocellular mechanisms.

Recently developed psychophysical techniques permit the biasing of the processing of the stimulus by early visual channels so that responses reflect characteristics of either magno- or parvocellular pathways (Pokorny & Smith, 1997). We used such techniques to test psychophysically whether the global magnocellular dysfunction reported in schizophrenia also affects early processes. Seven schizophrenic patients and 19 normal controls participated. The task was a four-alternative forced-choice luminance discrimination, using a 2 × 2 configuration of four 1-deg squares. Target luminance threshold was determined in three conditions: the stimulus, including the target, was pulsed for 17 ms (pulse paradigm); the target was presented on a steady background of four squares (steady paradigm), or the target was presented alone (no background paradigm). We replicated previous results demonstrating magnocellular and parvocellular signatures in control participants. No evidence for an early magnocellular deficit could be detected as the thresholds of all schizophrenic observers were higher both in the steady paradigm (presumed magnocellular mediation) and in the pulse paradigm (presumed parvocellular mediation). Magnocellular dysfunction, if present in schizophrenia, must concern more integrated processes, possibly at levels at which parvocellular and magnocellular paths interact.

Many neurons in the primary visual cortex (area V1) show pronounced selectivity for the orientation and spatial frequency of visual stimuli, whereas most neurons in subcortical afferent streams show little selectivity for these stimulus attributes. It has been suggested that this transformation is a functional sign of increased coding efficiency, whereby the redundancy (or overlap in response properties) is reduced at consecutive levels of visual processing. Here we compared experimentally the response redundancy in area V1 with that in the three main dorsal thalamic afferent streams, the parvocellular (PC), koniocellular (KC), and magnocellular (MC) divisions of the dorsal lateral geniculate nucleus (LGN) in marmosets. The spatial frequency and orientation tuning of single cells in the LGN and area V1 were measured, using luminance contrast sine-wave gratings. A joint spatial frequency-orientation response selectivity profile was calculated for each cell. Response redundancy for each population was estimated by cross-multiplication of the joint selectivity profiles for pairs of cells. We show that when estimated in this way, redundancy in LGN neurons is approximately double that of neurons in cortical area V1. However, there are differences between LGN subdivisions, such that the KC pathway has a spatial representation that lies between the redundant code of the PC and MC pathways and the more efficient sparse spatial code of area V1.

The Zoellner illusion is a geometric distortion occurring when nonorthogonal inducing lines appear to tilt veridically parallel bars. The retinal pathways contributing to such illusions are unknown. The goal of this experiment was to investigate the retinal origin of the illusion. This was accomplished by determining the contrast gain for illusion thresholds. The magnocellular (MC-) and parvocellular (PC-) pathways exhibit different contrast gains, and this difference can be used psychophysically to identify the pathway. The stimulus pattern was four vertical bars with a series of inducing lines. The bars were always 5% higher in contrast than the inducing bars. The pattern was presented on a larger pedestal. Two paradigms were used. In the pulsed-pedestal paradigm, the observer adapted to the background and the pedestal and pattern were presented together as a brief pulse. In the steady-pedestal paradigm, the observer adapted to the continuously presented pedestal and the pattern appeared as a brief pulse. The contrast between the pedestal and the pattern was varied to obtain thresholds for two criteria: perceiving the directions of the inner inducing lines, and perceiving the distortion of the bars. The results for both criteria were similar in shape, but displaced in sensitivity. Detection of the directions of the inner inducing lines was 0.16–0.29 log unit more sensitive than perception of the illusion. The data for the pulsed-pedestal paradigm depended on the contrast between the pedestal and the pattern and produced a shallow V-shape. These results were associated with mediation in the PC-pathway. The data for the steady-pedestal paradigm depended on the pedestal luminance in a linear relation and showed similar sensitivity to the data for the pulsed-pedestal paradigm. Perception of the illusion required 10–15% Weber contrast.

Neurophysiological recordings have shown that activity of magnocellular neurons may be reduced by red backgrounds. This has led some researchers to use red light, or red filters, in attempts to determine the magnocellular contribution to psychophysical tasks. This requires that red light not affect parvocellular neurons, or at least that it is possible to control for the effect on the parvocellular system by using other colors. The present report investigates these assumptions by calculating the effect of red, green, and blue filters on the three cone pigments and on the four parvocellular color-opponent cell mechanisms. It is found that a red filter has a large effect on the long- and middle-wavelength cone pigments and on the red–green color-opponent mechanisms. A green filter, on the other hand, has little effect. A blue filter has a fairly pronounced effect but this effect is distinctly different from that of the red filter. These results indicate that one ought not rely upon red light to isolate magnocellular activity in psychological experiments. The results also indicate that it is difficult to use colors other than red to control for the effect of this color on the parvocellular system.

A labeled ON parasol ganglion cell from a macaque retina was analyzed in serial, ultrathin sections. It received 13% of its input from diffuse bipolar cells. These directed a large proportion of their output to amacrine cells but received a relatively small proportion of their amacrine cell input via feedback synapses. In these respects, they were similar to the DB3 bipolar cells that make synapses onto OFF parasol cells. Bipolar cell axons that contacted the ON parasol cell in stratum 4 of the inner plexiform layer always made synapses onto the dendrite, and therefore, the number of bipolar cell synapses onto these ganglion cells could be estimated reliably by light microscopy in the future. Amacrine cells provided the majority of inputs to the ON parasol cell. Only a few of the presynaptic amacrine cell processes received inputs from the same bipolar cells as the parasol cells, and most of the presynaptic amacrine cell processes did not receive any inputs at all within the series. These findings suggest that most of the inhibitory input to the ON parasol cell originates from other areas of the retina. Amacrine cells presynaptic to the parasol ganglion cell interacted very infrequently with other neurons in the circuit, and therefore, they would be expected to act independently, for the most part.

There is considerable controversy over the existence of orientation and direction sensitivity in lateral geniculate nucleus (LGN) neurons. Claims for the existence of these properties often were based upon data from cells tested well beyond their peak spatial frequencies. The goals of the present study were to examine the degree of orientation and direction sensitivity of LGN cells when tested at their peak spatial and temporal frequencies and to compare the tuning properties of these subcortical neurons with those of visual cortex. For this investigation, we used conventional extracellular recording to study orientation and direction sensitivities of owl monkey LGN cells by stimulating cells with drifting sinusoidal gratings at peak temporal frequencies, peak or higher spatial frequencies, and moderate contrast. A total of 110 LGN cells (32 koniocellular cells, 34 magnocellular cells, and 44 parvocellular cells) with eccentricities ranging from 2.6 deg to 27.5 deg were examined. Using the peak spatial and temporal frequencies for each cell, 41.8% of the LGN cells were found to be sensitive to orientation and 19.1% were direction sensitive. The degree of bias for orientation and direction did not vary with eccentricity or with cell class. Orientation sensitivity did, however, increase, and in some cases orientation preferences changed, at higher spatial frequencies. Increasing spatial frequency had no consistent effect on direction sensitivity. Compared to cortical cell orientation tuning, the prevalence and strength of LGN cell orientation and direction sensitivity are weak. Nevertheless, the high percentage of LGN cells sensitive to orientation even at peak spatial and temporal frequencies reinforces the view that subcortical biases could, in combination with activity-dependent cortical mechanisms and/or cortical inhibitory mechanisms, account for the much narrower orientation and direction tuning seen in visual cortex.

The inhibitory neurotransmitter gamma aminobutyric acid (GABA) has been shown to influence the responses of ganglion cells in the mammalian retina. Consistently, GABAA receptor subunits have been localized to different ganglion cell types. In this study, the distribution of the α1 subunit of the GABAA receptor on the dendrites of midget and parasol ganglion cells was investigated quantitatively in the retina of a New World monkey, the marmoset. Ganglion cells were injected with Neurobiotin in a live in vitro retinal whole-mount preparation. Retinal pieces were then processed with an antibody against the α1 subunit of the GABAA receptor. Strong punctate immunoreactivity indicative of synaptic localization is present in the ON and OFF sublamina of the inner plexiform layer. Many of the immunoreactive puncta coincide with the dendrites of both midget and parasol ganglion cells. Immunoreactive puncta are present on distal and proximal dendrites of ON and OFF cells of both ganglion cell types. On average, parasol cells show a slight increase in the spatial density of immunoreactive puncta with distance from the soma, whereas the density of immunoreactive puncta on midget cells stays even. Parasol ganglion cells show a slightly higher average density of immunoreactive puncta (0.083 puncta/μm dendrite) than midget cells (0.054 puncta/μm dendrite).

Signals relayed through the magnocellular layers of the LGN travel on axons with faster conduction speeds than those relayed through the parvocellular layers. As a result, magnocellular signals might reach cerebral cortex appreciably before parvocellular signals. The relative speed of these two channels cannot be accurately predicted based solely on axon conduction speeds, however. Other factors, such as different degrees of convergence in the magnocellular and parvocellular channels and the retinal circuits that feed them, can affect the time it takes for magnocellular and parvocellular signals to activate cortical neurons. We have investigated the relative timing of visual responses mediated by the magnocellular and parvocellular channels. We recorded individually from 78 magnocellular and 80 parvocellular neurons in the LGN of two anesthetized monkeys. Visual response latencies were measured for small spots of light of various intensities. Over a wide range of stimulus intensities the fastest magnocellular response latencies preceded the fastest parvocellular response latencies by about 10 ms. Because parvocellular neurons are far more numerous than magnocellular neurons, convergence in cortex could reduce the magnocellular advantage by allowing parvocellular signals to generate detectable responses sooner than expected based on the responses of individual parvocellular neurons. An analysis based on a simple model using neurophysiological data collected from the LGN shows that convergence in cortex could eliminate or reverse the magnocellular advantage. This observation calls into question inferences that have been made about ordinal relationships of neurons based on timing of responses.