Responses to contour features in macaque area V4.
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The ventral pathway in visual cortex is responsible for the perception of shape. Area V4 is an important intermediate stage in this pathway, and provides the major input to the final stages in inferotemporal cortex. The role of V4 in processing shape information is not yet clear. We studied V4 responses to contour features (angles and curves), which many theorists have proposed as intermediate shape primitives. We used a large parametric set of contour features to test the responses of 152 V4 cells in two awake macaque monkeys. Most cells responded better to contour features than to edges or bars, and about one-third exhibited systematic tuning for contour features. In particular, many cells were selective for contour feature orientation, responding to angles and curves pointing in a particular direction. There was a strong bias toward convex (as opposed to concave) features, implying a neural basis for the well-known perceptual dominance of convexity. Our results suggest that V4 processes information about contour features as a step toward complex shape recognition. (+info)
Quantitative analysis of abducens neuron discharge dynamics during saccadic and slow eye movements.
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The mechanics of the eyeball and its surrounding tissues, which together form the oculomotor plant, have been shown to be the same for smooth pursuit and saccadic eye movements. Hence it was postulated that similar signals would be carried by motoneurons during slow and rapid eye movements. In the present study, we directly addressed this proposal by determining which eye movement-based models best describe the discharge dynamics of primate abducens neurons during a variety of eye movement behaviors. We first characterized abducens neuron spike trains, as has been classically done, during fixation and sinusoidal smooth pursuit. We then systematically analyzed the discharge dynamics of abducens neurons during and following saccades, during step-ramp pursuit and during high velocity slow-phase vestibular nystagmus. We found that the commonly utilized first-order description of abducens neuron firing rates (FR = b + kE + r, where FR is firing rate, E and are eye position and velocity, respectively, and b, k, and r are constants) provided an adequate model of neuronal activity during saccades, smooth pursuit, and slow phase vestibular nystagmus. However, the use of a second-order model, which included an exponentially decaying term or "slide" (FR = b + kE + r + uE - c), notably improved our ability to describe neuronal activity when the eye was moving and also enabled us to model abducens neuron discharges during the postsaccadic interval. We also found that, for a given model, a single set of parameters could not be used to describe neuronal firing rates during both slow and rapid eye movements. Specifically, the eye velocity and position coefficients (r and k in the above models, respectively) consistently decreased as a function of the mean (and peak) eye velocity that was generated. In contrast, the bias (b, firing rate when looking straight ahead) invariably increased with eye velocity. Although these trends are likely to reflect, in part, nonlinearities that are intrinsic to the extraocular muscles, we propose that these results can also be explained by considering the time-varying resistance to movement that is generated by the antagonist muscle. We conclude that to create realistic and meaningful models of the neural control of horizontal eye movements, it is essential to consider the activation of the antagonist, as well as agonist motoneuron pools. (+info)
Apparent dissociation between saccadic eye movements and the firing patterns of premotor neurons and motoneurons.
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Saccadic eye movements result from high-frequency bursts of activity in ocular motoneurons. This phasic activity originates in premotor burst neurons. When the head is restrained, the number of action potentials in the bursts of burst neurons and motoneurons increases linearly with eye movement amplitude. However, when the head is unrestrained, the number of action potentials now increase as a function of the change in the direction of the line of sight during eye movements of relatively similar amplitudes. These data suggest an apparent uncoupling of premotor neuron and motoneuron activity from the resultant eye movement. (+info)
Visual field defects associated with vigabatrin therapy.
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OBJECTIVE: To estimate the prevalence of visual field defects in patients taking the anticonvulsant drug vigabatrin and to characterise the features of visual dysfunction found. METHODS: Thirty three unselected patients attending neurology and epilepsy clinics were identified as taking vigabatrin and asked to attend for neuro-ophthalmic evaluation. A control group of 16 patients with epilepsy unexposed to vigabatrin was also evaluated. Visual fields were examined by static perimetry using a Humphrey field analyser. Patients underwent detailed ophthalmic examination, various blood tests, and brain MRI where necessary. Visual evoked responses (VERs), electro-oculograms (EOGs), and electroretinograms (ERGs) were recorded. RESULTS: Of 31 assessable patients treated with vigabatrin, 16 (52%) had definitely abnormal visual fields, nine (29%) had fields that were inconclusive, four (13%) had normal fields, and two (6%) proved unable to cooperate with testing. In four patients some plausible cause was found for the field abnormality leaving 12 patients (39%) in whom a definite bilateral field defect was found, possibly caused by vigabatrin treatment. Of 16 control patients none had definitely abnormal fields, 12 (75%) had normal fields, and four (25%) had fields that were inconclusive. The field defects associated with vigabatrin treatment showed a characteristic pattern of concentric peripheral field loss with temporal and macular sparing. The VERs and ERGs were normal. The EOG Arden Index was reduced in patients taking vigabatrin, although this returned towards normal when vigabatrin was stopped, even in the presence of persistent field defects. Multifocal ERGs recorded in two patients were abnormal, showing marked reduction in amplitude of the peripheral focal ERG. CONCLUSIONS: Treatment with vigabatrin was associated with a high prevalence of peripheral visual field defects. This seemed to be the result of a toxic effect of vigabatrin on the retina and seemed to persist if the drug was withdrawn. (+info)
Using response models to estimate channel capacity for neuronal classification of stationary visual stimuli using temporal coding.
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Both spike count and temporal modulation are known to carry information about which of a set of stimuli elicited a response; but how much information temporal modulation adds remains a subject of debate. This question usually is addressed by examining the results of a particular experiment that depend on the specific stimuli used. Developing a response model allows us to ask how much more information is carried by the best use of response strength and temporal modulation together (that is, the channel capacity using a code incorporating both) than by the best use of spike count alone (the channel capacity using the spike count code). This replaces dependence on a particular data set with dependence on the accuracy of the model. The model is constructed by finding statistical rules obeyed by all the observed responses and assuming that responses to stimuli not presented in our experiments obey the same rules. We assume that all responses within the observed dynamic range, even if not elicited by a stimulus in our experiment, could be elicited by some stimulus. The model used here is based on principal component analysis and includes both response strength and a coarse (+/-10 ms) representation of temporal modulation. Temporal modulation at finer time scales carries little information about the identity of stationary visual stimuli (although it may carry information about stimulus motion or change), and we present evidence that, given its variability, it should not be expected to do so. The model makes use of a linear relation between the logarithms of mean and variance of responses, similar to the widely seen relation between mean and variance of spike count. Responses are modeled using truncated Gaussian distributions. The amount of stimulus-related information carried by spike count in our data are 0.35 and 0.31 bits in primary visual and inferior temporal cortices, respectively, rising to 0.52 and 0.37 bits for the two-principal-component code. The response model estimates that the channel capacity is 1.1 and 1.4 bits, respectively, using the spike count only, rising to 2.0 and 2.2 bits using two principal components. Thus using this representation of temporal modulation is nearly equivalent to adding a second independent cell using the spike count code. This is much more than estimated using transmitted information but far less than would be expected if all degrees of freedom provided by the individual spike times carried independent information. (+info)
Comparison of saccades perturbed by stimulation of the rostral superior colliculus, the caudal superior colliculus, and the omnipause neuron region.
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Over the past decade, considerable research efforts have been focused on the role of the rostral superior colliculus (SC) in control of saccades. The most recent theory separates the deeper intermediate layers of the SC into two functional regions: the rostral pole of these layers constitutes a fixation zone and the caudal region comprises the saccade zone. Sustained activity of fixation neurons in the fixation zone is argued to maintain fixation and help prevent saccade generation by exciting the omnipause neurons (OPNs) in the brain stem. This hypothesis is in contrast to the traditional view that the SC contains a topographic representation of the saccade motor map on which the rostral pole of the SC encodes signals for generating small saccades (<2 degrees ) instead of preventing them. There is therefore an unresolved controversy about the specific role on the most rostral region of the SC, and we reexamined its functional contribution by quantifying and comparing spatial and temporal trajectories of 30 degrees saccades perturbed by electrical stimulation of the rostral pole and more caudal regions in the SC and of the OPN region. If the rostral pole serves to preserve fixation, then saccades perturbed by stimulation should closely resemble interrupted saccades produced by stimulation of the OPN region. If it also contributes to saccade generation, then the disrupted movements would better compare with redirected saccades observed after stimulation of the caudal SC. Our experiments revealed two significant findings: 1) the locus of stimulation was the primary factor determining the perturbation effect. If the directions of the target-directed saccade and stimulation-evoked saccade were aligned and if the stimulation was delivered within approximately the rostral 2 mm (<10 degrees amplitude) of SC, the ongoing saccade stopped in midflight but then resumed after stimulation end to reach the original visually specified goal with close to normal accuracy. When stimulation was applied at more caudal sites, the ongoing saccade directly reached the target location without stopping at an intermediate position. If the directions differed considerably, both initial and resumed components were typically observed for all stimulation sites. 2) A quantitative analysis of the saccades perturbed from the fixation zone showed significant deviations from their control spatial trajectories. Thus they resembled redirected saccades induced by caudal SC stimulation and differed significantly from interrupted saccades produced by OPN stimulation. The amplitude of the initial saccade, latency of perturbation, and spatial redirection were greatest for the most caudal sites and decreased gradually for rostral sites. For stimulation sites within the rostral pole of SC, the measures formed a smooth continuation of the trends observed in the saccade zone. As these results argue for the saccade zone concept, we offer reinterpretations of the data used to support the fixation zone model. However, we also discuss scenarios that do not allow an outright rejection of the fixation zone hypothesis. (+info)
Quantitative analysis of substantia nigra pars reticulata activity during a visually guided saccade task.
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Several lines of evidence suggest that the pars reticulata subdivision of the substantia nigra (SNr) plays a role in the generation of saccadic eye movements. However, the responses of SNr neurons during saccades have not been examined with the same level of quantitative detail as the responses of neurons in other key saccadic areas. For this report, we examined the firing rates of 72 SNr neurons while awake-behaving primates correctly performed an average of 136 trials of a visually guided delayed saccade task. On each trial, the location of the visual target was chosen randomly from a grid spanning 40 degrees of horizontal and vertical visual angle. We measured the firing rates of each neuron during five intervals on every trial: a baseline interval, a fixation interval, a visual interval, a movement interval, and a reward interval. We found four distinct classes of SNr neurons. Two classes of neurons had firing rates that decreased during delayed saccade trials. The firing rates of discrete pausers decreased after the onset of a contralateral target and/or before the onset of a saccade that would align gaze with that target. The firing rates of universal pausers decreased after fixation on all trials and remained below baseline until the delivery of reinforcement. We also found two classes of SNr neurons with firing rates that increased during delayed saccade trials. The firing rates of bursters increased after the onset of a contralateral target and/or before the onset of a saccade aligning gaze with that target. The firing rates of pause-bursters increased after the onset of a contralateral target but decreased after the illumination of an ipsilateral target. Our quantification of the response profiles of SNr neurons yielded three novel findings. First, we found that some SNr neurons generate saccade-related increases in activity. Second, we found that, for nearly all SNr neurons, the relationship between firing rate and horizontal and vertical saccade amplitude could be well described by a planar surface within the range of movements we sampled. Finally we found that for most SNr neurons, saccade-related modulations in activity were highly variable on a trial-by-trial basis. (+info)
Monocular occlusion can improve binocular control and reading in dyslexics.
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Developmental dyslexia is a neurodevelopmental condition which causes 5-10% of children to have unexpected difficulty learning to read. Many dyslexics have impaired development of the magnocellular component of the visual system, which is important for timing visual events and controlling eye movements. Poor control of eye movement may lead to unstable binocular fixation, and hence unsteady vision; this could explain why many dyslexics report that letters appear to move around, causing visual confusion. Previous research has suggested that such binocular confusion can be permanently alleviated by temporarily occluding one eye. The aim of the present study was therefore to assess the binocular control and reading progress of dyslexic children with initially unstable binocular control after the left eye was patched. One hundred and forty-three dyslexics were studied. They were selected from children aged 7-11 years referred to a learning disabilities clinic if they were dyslexic and had unstable binocular control. They were randomly assigned to wear yellow spectacles with or without the left lens occluded, and were followed for 9 months. Significantly more of the children who were given occlusion gained stable binocular fixation in the first 3 months (59%) compared with children given the unoccluded glasses (36%). This advantage was independent of IQ or initial reading ability. Furthermore, at all the 3-month follow-ups, children were more likely to have gained stable binocular control if they had been wearing the occluded glasses. Gaining stable binocular control significantly improved reading. The children who did so with the help of occlusion improved their reading by 9.4 months in the first 3 months, compared with 3.9 months in those who were not patched and did not gain stable fixation. Over the whole 9 months, children who received occlusion and gained stable fixation nearly doubled their rate of progress in reading compared with those who remained unstable. At all the follow-ups the reading of those given occlusion was significantly better than that of those not occluded. Thus monocular occlusion helped children with unstable binocular control to gain good binocular fixation. If they gained stability, they made significantly faster reading progress. The progress made by the children who gained stable fixation was much greater than that achieved with other remedial techniques. (+info)