scholarly journals The responses of V1 cortical neurons to flashed presentations of orthogonal single lines and edges

2015 ◽  
Vol 113 (7) ◽  
pp. 2676-2681 ◽  
Author(s):  
Timothy J. Gawne
Keyword(s):  
Cortical Neurons ◽  
Weighted Average ◽  
Gain Control ◽  
Control Mechanisms ◽  
Strong Suppression ◽  
V1 Neurons ◽  
Contrast Gain ◽  
Oriented Stimulus ◽  
Visual Cortical Area ◽  
Visual Cortical

How cortical neurons process multiple inputs is a fundamental issue in modern neuroscience. Neurons in visual cortical area V1 have been shown to exhibit cross-orientation suppression, where the response to an optimally oriented visual stimulus is reduced by the simultaneous presence of an orthogonally oriented stimulus. This is consistent with the view that cortical neurons respond to multiple inputs with a weighted average (or normalization) of the responses to the inputs presented separately. However, most of these studies have used drifting or counterphase-modulated grating stimuli, potentially confounding orientation effects with non-orientation-specific gain control mechanisms. Additionally, primate vision depends to a great extent on transient stimulus presentations during fixations between saccades. Therefore this study examined the responses of primate V1 neurons to orthogonal flashed-onset single edges and lines, and to their combinations. Single edges or lines do not typically cause strong suppression of the responses to an orthogonal stimulus, even though a grating does. This appears to hold true regardless of the relative contrasts of the orthogonal single lines or edges. This is consistent with response suppression from an orthogonal grating being due to non-orientation-specific contrast gain control (Koeling M, Shapley R, Shelley M. J Comp Neurosci 25: 390–400, 2008; Priebe NJ, Ferster D. Nat Neurosci 9: 552–561, 2006; Walker GA, Ohzawa I, Freeman RD. J.Neurophysiol 79: 227–239, 1998). While normalization mechanisms are clearly important for the cerebral cortex, under many conditions the responses of V1 cortical neurons to an optimally oriented stimulus can be unaffected by the presence of orthogonal stimuli, which may be important to avoid confounding the interpretation of a neural response.

Activity of Primate V1 Cortical Neurons During Blinks

2000 ◽  
Vol 84 (5) ◽  
pp. 2691-2694 ◽  
Author(s):  
Timothy J. Gawne ◽  
Julie M. Martin
Keyword(s):  
Neuronal Activity ◽  
Visual Stimulus ◽  
Cortical Neurons ◽  
Cortical Area ◽  
Constant Stimulus ◽  
V1 Neurons ◽  
Reflex Blink ◽  
Visual Cortical Area ◽  
Electrooptical Shutter ◽  
Visual Cortical

Every time we blink our eyes, the image on the retina goes almost completely dark. And yet we hardly notice these interruptions, even though an external darkening is startling. Intuitively it would seem that if our perception is continuous, then the neuronal activity on which our perceptions are based should also be continuous. To explore this issue, we compared the responses of 63 supragranular V1 neurons recorded from two awake monkeys for four conditions: 1) constant stimulus, 2) during a reflex blink, 3) during a gap in the visual stimulus, and 4) during an external darkening when an electrooptical shutter occluded the entire scene. We show here that the activity of neurons in visual cortical area V1 is essentially shut off during a blink. In the 100-ms epoch starting 70 ms after the stimulus was interrupted, the firing rate was 27.2 ± 2.7 spikes/s (SE) for a constant stimulus, 8.2 ± 0.9 spikes/s for a reflex blink, 17.3 ± 1.9 spikes/s for a gap, and 12.7 ± 1.4 spikes/s for an external darkening. The responses during a blink are less than during an external darkening ( P < 0.05, t-test). However, many of these neurons responded with a transient burst of activity to the onset of an external darkening and not to a blink, suggesting that it is the suppression of this transient which causes us to ignore blinks. This is consistent with other studies where the presence of transient bursts of activity correlates with the perceived visibility of a stimulus.

Development of visual inhibitory interactions in kittens

1991 ◽  
Vol 7 (4) ◽  
pp. 321-334 ◽  
Author(s):  
M. Concetta Morrone ◽  
Harriet D. Speed ◽  
David C. Burr
Keyword(s):  
Second Harmonic ◽  
Gain Control ◽  
Contrast Threshold ◽  
Control Mechanisms ◽  
Response Curves ◽  
Contrast Gain ◽  
Visual Neurones ◽  
Adult Cats ◽  
Contrast Response ◽  
Inhibitory Interactions

AbstractThis study was designed to monitor the development of inhibitory interactions elicited in the cat visual system by oriented visual stimuli. Steady-state visual-evoked potentials (VEPs) were recorded from the scalp of 11 behaving and alert kittens while they viewed contrast-reversed sinusoidal gratings. In adult cats, the form of VEP contrast-response curves (the amplitude of second harmonic modulation as a function of stimulus contrast) was modified by superimposing a mask grating on the test. Parallel masks displaced the curves to a higher contrast region (probably via contrast gain-control mechanisms), increasing contrast threshold without affecting the slope of the curve. Orthogonal gratings, on the other hand, decrease the slope of the curve without affecting threshold (so called cross-orientation inhibition: Morrone et al., 1981). These effects are similar to those previously reported in human VEPs (Morrone & Burr, 1986; Burr & Morrone, 1987) and single cortical cat cells (Morrone et al., 1982). For young kittens of 20 days, the orthogonal mask had no effect whatsoever on the response curves, and the effect of the parallel mask was much less than for adult cats. At about 40 days, the orthogonal mask began to attenuate responses multiplicatively, and by 50 days the amount of multiplicative attenuation had reached adult levels. The effect of the parallel mask (as indicated by the increase in threshold elevation) increased gradually from 20–50 days. The results are consistent with the existence of at least two types of inhibition in cat visual neurones that develop at different rates.

scholarly journals Systematic misestimation in a vernier task arising from contrast mismatch

2008 ◽  
Vol 25 (3) ◽  
pp. 365-370 ◽  
Author(s):  
HAO SUN ◽  
BARRY B. LEE ◽  
RIGMOR C. BARAAS
Keyword(s):  
Ganglion Cells ◽  
Gain Control ◽  
Phase Advance ◽  
Target Pair ◽  
Control Mechanisms ◽  
Low Contrast ◽  
Contrast Gain ◽  
Contrast Gain Control ◽  
Cell Responses ◽  
High Contrast Grating

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.

The response dynamics of primate visual cortical neurons to simulated optical blur

2009 ◽  
Vol 26 (4) ◽  
pp. 411-420 ◽  
Author(s):  
MICHAEL L. RISNER ◽  
TIMOTHY J. GAWNE
Keyword(s):  
Cortical Neurons ◽  
Receptive Fields ◽  
Luminance Contrast ◽  
Form Perception ◽  
Response Dynamics ◽  
V1 Neurons ◽  
Spatial Frequencies ◽  
Wide Range ◽  
Optical Blur ◽  
Visual Cortical

AbstractNeurons in visual cortical area V1 typically respond well to lines or edges of specific orientations. There have been many studies investigating how the responses of these neurons to an oriented edge are affected by changes in luminance contrast. However, in natural images, edges vary not only in contrast but also in the degree of blur, both because of changes in focus and also because shadows are not sharp. The effect of blur on the response dynamics of visual cortical neurons has not been explored. We presented luminance-defined single edges in the receptive fields of parafoveal (1–6 deg eccentric) V1 neurons of two macaque monkeys trained to fixate a spot of light. We varied the width of the blurred region of the edge stimuli up to 0.36 deg of visual angle. Even though the neurons responded robustly to stimuli that only contained high spatial frequencies and 0.36 deg is much larger than the limits of acuity at this eccentricity, changing the degree of blur had minimal effect on the responses of these neurons to the edge. Primates need to measure blur at the fovea to evaluate image quality and control accommodation, but this might only involve a specialist subpopulation of neurons. If visual cortical neurons in general responded differently to sharp and blurred stimuli, then this could provide a cue for form perception, for example, by helping to disambiguate the luminance edges created by real objects from those created by shadows. On the other hand, it might be important to avoid the distraction of changing blur as objects move in and out of the plane of fixation. Our results support the latter hypothesis: the responses of parafoveal V1 neurons are largely unaffected by changes in blur over a wide range.

Cortical neurons: Isolation of contrast gain control

1992 ◽  
Vol 32 (8) ◽  
pp. 1409-1410 ◽  
Author(s):  
Wilson S. Geisler ◽  
Duane G. Albrecht
Keyword(s):  
Cortical Neurons ◽  
Gain Control ◽  
Contrast Gain ◽  
Contrast Gain Control

scholarly journals Gain control from beyond the classical receptive field in primate primary visual cortex

2003 ◽  
Vol 20 (3) ◽  
pp. 221-230 ◽  
Author(s):  
BEN S. WEBB ◽  
CHRIS J. TINSLEY ◽  
NICK E. BARRACLOUGH ◽  
AMANDA PARKER ◽  
ANDREW M. DERRINGTON
Keyword(s):  
Visual Cortex ◽  
Receptive Field ◽  
Primary Visual Cortex ◽  
Gain Control ◽  
Salient Feature ◽  
Retinal Eccentricity ◽  
V1 Neurons ◽  
Contrast Gain ◽  
Classical Receptive Field ◽  
Extrastriate Areas

Gain control is a salient feature of information processing throughout the visual system. Heeger (1991, 1992) described a mechanism that could underpin gain control in primary visual cortex (V1). According to this model, a neuron's response is normalized by dividing its output by the sum of a population of neurons, which are selective for orientations covering a broad range. Gain control in this scheme is manifested as a change in the semisaturation constant (contrast gain) of a V1 neuron. Here we examine how flanking and annular gratings of the same or orthogonal orientation to that preferred by a neuron presented beyond the receptive field modulate gain in V1 neurons in anesthetized marmosets (Callithrix jacchus). To characterize how gain was modulated by surround stimuli, the Michaelis–Menten equation was fitted to response versus contrast functions obtained under each stimulus condition. The modulation of gain by surround stimuli was modelled best as a divisive reduction in response gain. Response gain varied with the orientation of surround stimuli, but was reduced most when the orientation of a large annular grating beyond the classical receptive field matched the preferred orientation of neurons. The strength of surround suppression did not vary significantly with retinal eccentricity or laminar distribution. In the marmoset, as in macaques (Angelucci et al., 2002a, b), gain control over the sort of distances reported here (up to 10 deg) may be mediated by feedback from extrastriate areas.

Contrast gain control in the cat's visual system

1985 ◽  
Vol 54 (3) ◽  
pp. 651-667 ◽  
Author(s):  
I. Ohzawa ◽  
G. Sclar ◽  
R. D. Freeman
Keyword(s):  
Contrast Sensitivity ◽  
Cortical Neurons ◽  
Time Course ◽  
Gain Control ◽  
Local Contrast ◽  
Response Functions ◽  
Contrast Gain ◽  
Contrast Gain Control ◽  
Contrast Adaptation ◽  
Contrast Response

We have examined the idea that the adaptation of cortical neurons to local contrast levels in a visual stimulus is functionally advantageous. Specifically, cortical cells may have large differential contrast sensitivity as a result of adjustments that center a limited response range around a mean level of contrast. To evaluate this notion, we measured contrast-response functions of cells in striate cortex while systematically adapting them to different contrast levels of stimulus gratings. For the majority of cortical neurons tested, the results of this basic experiment show that contrast-response functions shift laterally along a log-contrast axis so that response functions match mean contrast levels in the stimulus. This implies a contrast-dependent change in the gain of the cell's contrast-response relationship. We define this process as contrast gain control. The degree to which this contrast adjustment occurs varies considerably from cell to cell. There are no obvious differences regarding cell type (simple vs. complex) or laminar distribution. Contrast gain control is almost certainly a cortical function, since lateral geniculate cells and fibers exhibit only minimal effects. Tests presented in the accompanying paper (37) provide additional evidence on the cortical origin of the process. In another series of experiments, the effect of contrast adaptation on physiological estimates of contrast sensitivity was evaluated. Sustained adaptation to contrast levels as low as 3% was capable of nearly doubling the thresholds of most of the cells tested. Adaptation may therefore be an important factor in determinations of the contrast sensitivity of cortical neurons. We tested the spatial extent of the mechanisms responsible for these gain-control effects by attempting to adapt cells using both a large grating and a grating patch limited to that portion of a cell's receptive field from which excitatory discharges could be elicited directly (the central discharge region). Adaptation was found to be an exclusive property of the central region. This held even in the case of hypercomplex cells, which received strong influences from surrounding regions of the visual field. Finally, we measured the time course of contrast adaptation. We found the process to be rather slow, with a mean time constant of approximately 6 s. Once again, there was considerable variability in this value from cell to cell.

Stimulus-Dependent Modulation of Spike Burst Length in Cat Striate Cortical Cells

1997 ◽  
Vol 78 (1) ◽  
pp. 199-213 ◽  
Author(s):  
B. C. Debusk ◽  
E. J. Debruyn ◽  
R. K. Snider ◽  
J. F. Kabara ◽  
A. B. Bonds
Keyword(s):  
Firing Rate ◽  
Cortical Neurons ◽  
Nonlinear Function ◽  
Gain Control ◽  
Recurrent Network ◽  
Burst Frequency ◽  
Cortical Cells ◽  
Spike Burst ◽  
Burst Length ◽  
Contrast Gain

DeBusk, B. C., E. J. DeBruyn, R. K. Snider, J. F. Kabara, and A. B. Bonds. Stimulus-dependent modulation of spike burst length in cat striate cortical cells. J. Neurophysiol. 78: 199–213, 1997. Burst activity, defined by groups of two or more spikes with intervals of ≤8 ms, was analyzed in responses to drifting sinewave gratings elicited from striate cortical neurons in anesthetized cats. Bursting varied broadly across a population of 507 simple and complex cells. Half of this population had ≥42% of their spikes contained in bursts. The fraction of spikes in bursts did not vary as a function of average firing rate and was stationary over time. Peaks in the interspike interval histograms were found at both 3–5 ms and 10–30 ms. In many cells the locations of these peaks were independent of firing rate, indicating a quantized control of firing behavior at two different time scales. The activity at the shorter time scale most likely results from intrinsic properties of the cell membrane, and that at the longer scale from recurrent network excitation. Burst frequency (bursts per s) and burst length (spikes per burst) both depended on firing rate. Burst frequency was essentially linear with firing rate, whereas burst length was a nonlinear function of firing rate and was also governed by stimulus orientation. At a given firing rate, burst length was greater for optimal orientations than for nonoptimal orientations. No organized orientation dependence was seen in bursts from lateral geniculate nucleus cells. Activation of cortical contrast gain control at low response amplitudes resulted in no burst length modulation, but burst shortening at optimal orientations was found in responses characterized by supersaturation. At a given firing rate, cortical burst length was shortened by microinjection of γ-aminobutyric acid (GABA), and bursts became longer in the presence of N-methyl-bicuculline, a GABAA receptor blocker. These results are consistent with a model in which responses are reduced at nonoptimal orientations, at least in part, by burst shortening that is mediated by GABA. A similar mechanism contributes to response supersaturation at high contrasts via recruitment of inhibitory responses that are tuned to adjacent orientations. Burst length modulation can serve as a form of coding by supporting dynamic, stimulus-dependent reorganization of the effectiveness of individual network connections.

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