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Jenny C A Read

Publications and source records attributed to Jenny C A Read.

11 recordsLinked to original sources

Does depth perception require vertical-disparity detectors?

Stereo depth perception depends on the fact that objects project to different positions in the two eyes. Because our eyes are offset horizontally, these retinal disparities are mainly horizontal, and horizontal disparity suffices to give an impression of depth. However, depending on eye position, there may also be small vertical disparities. These are significant because, given both vertical and horizontal disparities, the brain can deduce eye position from purely retinal information and, hence, derive the position of objects in space. However, we show here that, to achieve this, the brain need measure only the magnitude of vertical disparity; for physically possible stimuli, the sign then follows from the stereo geometry. The magnitude of vertical disparity--and hence eye position--can be deduced from the response of purely horizontal-disparity sensors because vertical disparity moves corresponding features off the receptive fields, reducing the effective binocular correlation. As proof, we demonstrate an algorithm that can accurately reconstruct gaze and vergence angles from the population activity of pure horizontal-disparity sensors and show that it is subject to the induced effect. Given that disparities experienced during natural viewing are overwhelmingly horizontal and that eye position measures require only horizontal-disparity sensors, this work raises two questions: Does the brain in fact contain sensors tuned to nonzero vertical disparities, and if so, why?

Algorithms↗

Extracellular calcium regulates postsynaptic efficacy through group 1 metabotropic glutamate receptors.

Bursts of synaptic transmission are known to induce transient depletion of Ca2+ within the synaptic cleft. Although Ca2+ depletion has been shown to lower presynaptic release probability, effects on the postsynaptic cell have not been reported. In this study, we show that physiologically relevant reductions in extracellular Ca2+ lead to a decrease in synaptic strength between synaptically coupled layer 2/3 cortical pyramidal neurons. Using quantal analysis and mEPSP analysis, we demonstrate that a lowered extracellular Ca2+ produces a reduction in the postsynaptic quantal size in addition to its known effect on release probability. An elevated Mg2+ level can prevent this reduction in postsynaptic efficacy at subphysiological Ca2+ levels. We show that the calcium-dependent effect on postsynaptic quantal size is mediated by group 1 metabotropic glutamate receptors, acting via CaMKII (Ca2+/calmodulin-dependent protein kinase II) and PKC. Therefore, physiologically relevant changes in extracellular Ca2+ can regulate information transfer at cortical synapses via both presynaptic and postsynaptic mechanisms.

Animals↗

All Pulfrich-like illusions can be explained without joint encoding of motion and disparity.

In the Pulfrich effect, an interocular time delay results in the perception of depth. Two modified versions, the stroboscopic Pulfrich effect and dynamic visual noise with a delay, are generally explained by postulating an early stage of space/time-inseparable filtering, encoding motion and disparity jointly. However, most disparity sensors in monkey V1 do not show joint motion/disparity encoding, and we recently showed that depth perception in the stroboscopic Pulfrich effect is equally compatible with space/time-separable filtering. Here, we demonstrate that this filtering can be implemented with a population of physiologically plausible energy model units. Similar results are obtained whether the neurons are pure disparity sensors (like most V1 neurons) or joint motion/disparity sensors (like MT). We also demonstrate that the dynamic noise stimulus produces correlations between the activity in pure disparity sensors, and in a separate population of pure motion sensors. These correlations are sufficient to explain the percept. Thus, joint encoding of motion and disparity is not required to explain depth perception in Pulfrich-like stimuli: a brain which encoded motion and disparity in entirely separate neuronal pathways could still experience all of these illusions.

Animals↗

The stroboscopic Pulfrich effect is not evidence for the joint encoding of motion and depth.

In the Pulfrich effect, an illusion of depth is produced by introducing differences in the times at which a moving object is presented to the two eyes. In the classic form of the illusion, there is a simple explanation for the depth percept: the interocular delay introduces a spatial disparity into the stimulus. However, when the moving object is viewed stroboscopically, this simple explanation no longer holds. In recent years, depth perception in the stroboscopic Pulfrich effect has been explained by invoking neurons that are sensitive both to stereo disparity and to direction of motion. With such joint motion/disparity encoders, interocular delay causes a perception of depth by causing a shift in each neuron's preferred disparity. This model has been implemented by N. Qian and R. A. Andersen (1997). Here we show that this model's predictions for perceived disparity are quantitatively at odds with psychophysical measures. The joint-encoding model predicts that the perceived disparity is the virtual disparity implied by the apparent motion; in fact, the perceived disparity is smaller. We show that the percept can be quantitatively explained on the basis of spatial disparities present in the stimulus, which could be extracted from pure disparity sensors. These results suggest that joint encoding of motion and depth is not the dominant neuronal basis of depth perception in this stimulus.

Computer Simulation↗

Effect of interocular delay on disparity-selective v1 neurons: relationship to stereoacuity and the pulfrich effect.

The temporal properties of disparity-sensitive neurons place important temporal constraints on stereo matching. We examined these constraints by measuring the responses of disparity-selective neurons in striate cortex of awake behaving monkeys to random-dot stereograms that contained interocular delays. Disparity selectivity was gradually abolished by increasing interocular delay (when the delay exceeds the integration time, the inputs from the 2 eyes become uncorrelated). The amplitude of the disparity-selective response was a Gaussian function of interocular delay, with a mean of 16 ms (+/-5 ms, SD). Psychophysical measures of stereoacuity, in both monkey and human observers, showed a closely similar dependency on time, suggesting that temporal integration in V1 neurons is what determines psychophysical matching constraints over time. There was a slight but consistent asymmetry in the neuronal responses, as if the optimum stimulus is one in which the right stimulus leads by about 4 ms. Because all recordings were made in the left hemisphere, this probably reflects nasotemporal differences in conduction times; psychophysical data are compatible with this interpretation. In only a few neurons (5/72), interocular delay caused a change in the preferred disparity. Such tilted disparity/delay profiles have been invoked previously to explain depth perception in the stroboscopic version of the Pulfrich effect (and other variants). However, the great majority of the neurons did not show tilted disparity/delay profiles. This suggests that either the activity of these neurons is ignored when viewing Pulfrich stimuli, or that current theories relating neuronal properties to perception in the Pulfrich effect need to be reevaluated.

Action Potentials↗

Understanding the cortical specialization for horizontal disparity.

Because the eyes are displaced horizontally, binocular vision is inherently anisotropic. Recent experimental work has uncovered evidence of this anisotropy in primary visual cortex (V1): neurons respond over a wider range of horizontal than vertical disparity, regardless of their orientation tuning. This probably reflects the horizontally elongated distribution of two-dimensional disparity experienced by the visual system, but it conflicts with all existing models of disparity selectivity, in which the relative response range to vertical and horizontal disparities is determined by the preferred orientation. Potentially, this discrepancy could require us to abandon the widely held view that processing in V1 neurons is initially linear. Here, we show that these new experimental data can be reconciled with an initial linear stage; we present two physiologically plausible ways of extending existing models to achieve this. First, we allow neurons to receive input from multiple binocular subunits with different position disparities (previous models have assumed all subunits have identical position and phase disparity). Then we incorporate a form of divisive normalization, which has successfully explained many response properties of V1 neurons but has not previously been incorporated into a model of disparity selectivity. We show that either of these mechanisms decouples disparity tuning from orientation tuning and discuss how the models could be tested experimentally. This represents the first explanation of how the cortical specialization for horizontal disparity may be achieved.

Animals↗

Ocular dominance predicts neither strength nor class of disparity selectivity with random-dot stimuli in primate V1.

We address two unresolved issues concerning the coding of binocular disparity in primary visual cortex. Experimental studies and theoretical models have suggested a relationship between a cell's ocular dominance, assessed with monocular stimuli, and its tuning to binocular disparity. First, the disparity energy model of disparity selectivity suggests that there should be a correlation between ocular dominance and the strength of disparity tuning. Second, several studies have reported a relationship between ocular dominance and the shape of the disparity tuning curve, with cells dominated by one eye more likely to have disparity tuning of the tuned-inhibitory type. We investigated both of these relationships in single neurons recorded from the primary visual cortex of awake fixating macaques, using dynamic random-dot patterns as a stimulus. To classify disparity tuning curves quantitatively, we develop a new measure of symmetry, which can be applied to any function. We find no evidence for any correlation between ocular dominance and the nature of disparity tuning. This places constraints on the circuitry underlying disparity tuning.

Algorithms↗

Testing quantitative models of binocular disparity selectivity in primary visual cortex.

Disparity-selective neurons in striate cortex (V1) probably implement the initial processing that supports binocular vision. Recently, much progress has been made in understanding the computations that these neurons perform on retinal inputs. The binocular energy model has been highly successful in providing a simple theory of these computations. A key feature of the energy model is that it is linear until after inputs from the two eyes are combined. Recently, however, a modified version of the energy model, incorporating threshold nonlinearities before binocular combination, has been proposed to account for the weaker disparity tuning observed with anticorrelated stimuli. In this study, we present new data needed for a critical assessment of these two models. We compare two key predictions of the models with responses of disparity-selective neurons recorded from V1 of awake fixating monkeys. We find that the original energy model, and a family of generalizations retaining linear binocular combination, are quantitatively inconsistent with the response of V1 neurons. In contrast, the modified version incorporating threshold nonlinearities can explain both sets of observations. We conclude that the energy model can be reconciled with experimental observations by adding a threshold before binocular combination. This gives us the clearest picture yet of the computation being carried out by disparity-selective V1 neurons.

Action Potentials↗

Measuring V1 receptive fields despite eye movements in awake monkeys.

One difficulty with measuring receptive fields in the awake monkey is that even well-trained animals make small eye movements during fixation. These complicate the measurement of receptive fields by blurring out the region where a response is observed, causing underestimates of the ability of individual neurons to signal changes in stimulus position. In simple cells, this blurring may severely disrupt estimates of receptive field structure. An accurate measurement of eye movements would allow correction of this blurring. Scleral search coils have been used to provide such measurements, although little is known about their accuracy. We have devised a range of approaches to address this issue: implanting two coils into a single eye, exploiting the small size of V1 receptive fields and developing maximum-likelihood fitting techniques to extract receptive field parameters in the presence of eye movements. All our investigations lead to the same conclusion: our scleral search coils (which were not sutured to the globe) are subject to an error of approximately the same magnitude as the small eye movements which occur during fixation: SD approximately 0.1 degrees. This error is large enough to explain the SD of measured vergence in the absence of any real changes in vergence state. This, and a variety of other arguments, indicate that the real variation in vergence is much smaller than coil measurements suggest. These results suggest that monkeys, like humans, maintain very stable vergence. The error has a slower time course than fixational eye movements so that search coils report the difference in eye position between two consecutive trials more accurately than the eye position itself on either trial. Receptive field estimates are unlikely to be improved by assuming the coil record is veridical and correcting for eye position accordingly. However, receptive field parameters can reliably be determined by a fitting technique that allows for eye movements. It is possible that suturing coils to the globe reduces the artifacts, but no method has been available to demonstrate this. These receptive field measurements provide a general means by which the reliability of eye-position measurements can be assessed.

Animals↗

A Bayesian approach to the stereo correspondence problem.

I present a probabilistic approach to the stereo correspondence problem. Rather than trying to find a single solution in which each point in the left retina is assigned a partner in the right retina, all possible matches are considered simultaneously and assigned a probability of being correct. This approach is particularly suitable for stimuli where it is inappropriate to seek a unique partner for each retinal position--for instance, where objects occlude each other, as in Panum's limiting case. The probability assigned to each match is based on a Bayesian analysis previously developed to explain psychophysical data (Read, 2002). This provides a convenient way to incorporate constraints that enable the ill-posed correspondence problem to be solved. The resulting model behaves plausibly for a variety of different stimuli.

Bayes Theorem↗

A simple model accounts for the response of disparity-tuned V1 neurons to anticorrelated images.

Disparity-tuned cells in primary visual cortex (VI) are thought to play a significant role in the processing of stereoscopic depth. The disparity-specific responses of these neurons have been previously described by an energy model based on local, feedforward interactions. This model fails to predict the response to binocularly anticorrelated stimuli, in which images presented to left and right eyes have opposite contrasts. The original energy model predicts that anticorrelation should invert the disparity tuning curve (phase difference pi), with no change in the amplitude of the response. Experimentally, the amplitude tends to be reduced with anticorrelated stimuli and a spread of phase differences is observed, although phase differences near pi are the most common. These experimental observations could potentially reflect a modulation of the V1 signals by feedback from higher visual areas (because anticorrelated stimuli create a weaker or nonexistent stereoscopic depth sensation). This hypothesis could explain the effects on amplitude, but the spread of phase differences is harder to understand. Here, we demonstrate that changes in both amplitude and phase can be explained by a straightforward modification of the energy model that involves only local processing. Input from each eye is passed through a monocular simple cell, incorporating a threshold, before being combined at a binocular simple cell that feeds into the energy computation. Since this local feedforward model can explain the responses of complex cells to both correlated and anticorrelated stimuli, there is no need to invoke any influence of global stereoscopic matching.

Animals↗