| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Report
Howard Hughes Medical Institute and Vision Center Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037
Submitted 14 February 2003; accepted in final form 9 April 2003
 |
ABSTRACT |
|---|
|
70 ms. The
spectral tuning of this increase was roughly, but not exactly, consistent with
a pure luminance increase. We conclude that peripheral luminance increases can
evoke fixational saccades. |
|
INTRODUCTION |
|---|
|
; Kustov and Robinson
1996; Theeuwes et al.
1999). On the other hand, a subject may attend covertly to a
peripheral visual stimulus while maintaining visual fixation, indicating
disengagement of the attentional and saccadic systems (e.g.,
Posner et al. 1980). The
extent of this disengagement is unclear; for example, it is unknown whether
peripheral visual stimuli influence the occurrence of small-amplitude saccades
that occur naturally during fixation. The present experiments address this
issue.
Theeuwes et al. (1998,
1999) demonstrated that abrupt
onsets can attract visual attention and induce involuntary saccades. Subjects
in their task were instructed to make saccades to color-defined targets among
distractors. The sudden appearance of a distractor during the subject's
reaction time frequently attracted a short-latency saccade of which the
subject later claimed to be unaware. Theeuwes et al. hypothesized that these
short-latency saccades derive from a fast, reflexive pathway that initiates
saccades to novel stimuli even when such saccades are inappropriate.
Tse et al. (2002) asked
whether sudden onsets elicit reflexive eye movements in subjects instructed
explicitly to maintain fixation. In contrast to Theeuwes' result, they found
that subjects' eye positions were not related clearly to the occurrence of
sudden onsets. Their analysis, however, was restricted to mean eye position
and may therefore have masked important relationships between onsets and
saccade occurrences. We used a saccade-triggered analysis technique to assess
directly the impact of a visual stimulus on saccade initiations.
We studied small-amplitude saccades made by monkeys during fixation while a
visual stimulus flickered randomly in the periphery. Monkeys were rewarded for
maintaining their eye position within a small electronically defined window:
large-amplitude saccades arrested trials and resulted in brief time-out
periods. Cross-correlation of the stimulus sequence with the occurrence of
small saccades within the fixation window revealed a systematic relationship
between the two: on average, a fixational saccade followed a transient
increase in luminance at a latency of 70 ms. Saccade directions were
distributed broadly with a slight bias away from the stimulus. Our results
demonstrate that peripheral luminance increments can evoke saccades even when
the task demands do not require saccades at all.
|
|
METHODS |
|---|
|
Two monkeys (Macaca mulatta) served as subjects in these
experiments. In an initial surgical procedure, performed with sterile
technique and under general anesthesia, each monkey was implanted with a
stainless steel head post and monocular sceleral search coil
(Judge et al. 1980). During
experimental sessions, the head post was secured to a mating piece on the
monkeys' chair to eliminate head movements. Eye position was digitized at 250
Hz for off-line analysis. Experimental protocols were approved by the Salk
Institute Animal Care and Use Committee, and conform to U. S. Department of
Agriculture regulations and to the National Institutes of Health guidelines
for the humane care and use of laboratory animals.
Behavioral paradigm
Juice rewards were provided on a random schedule while the monkeys maintained fixation on a 0.2 x 0.2° black square presented against a gray background (CIE coordinates: x = 0.33, y = 0.33, 65 cd/m2) on a computer monitor (Sony F500). On stimulated trials, a 3° diam stimulus disk was presented at an eccentric location 500 ms after the monkeys acquired the fixation point. Importantly, the stimulus was irrelevant to the monkeys' behavior; rewards were given for fixation only, and the monkeys had never been trained to saccade to this stimulus or use it otherwise in any behavioral task. In some sessions, stimulated trials were randomly interleaved with nonstimulated trials, which proceeded identically except that the stimulus never appeared. If the eye position left a 1 x 1° electronically defined window surrounding the fixation point, the stimulus and fixation point disappeared and data collection ceased. After 1 s, the fixation point reappeared and the next trial began. Trials concluded also if the animal maintained fixation for 10 s whereupon a reward was given.
Visual stimulation
The color of the stimulus disk, which was determined by the intensities of the red, green, and blue monitor phosphors, changed randomly and independently on every screen refresh (every 10 ms), as illustrated in Fig. 1A. Phosphor intensities were drawn from independent quantized and truncated Gaussian distributions, shown in Fig. 1B. The mean intensity of each phosphor in the patch was identical to that phosphor's contribution to the background. In most experiments, the SD of each distribution was 9% of the range physically achievable. This range corresponds to luminance contrasts of 3.9, 11.5, and 2.5% for the red, green, and blue phosphors, respectively.
|
One monkey (monkey C) viewed the stimulus through a tunnel lined
with aluminum foil to increase retinal illuminance and stabilize adaptation
state (Chichilnisky and Wandel
1999). For this animal, the average position of the stimulus was
7° left and 1° below the fixation point. During most of these
sessions, electrodes were inserted transdurally to record the electrical
activity of visual cortical neurons. For monkey T, the stimulus was
presented consistently 7° to the right and 1° below the fixation point
and electrodes were not inserted. Figure
1C illustrates the distribution of stimulus positions.
The foil-lined tunnel was omitted for monkey T to control for the
possibility that results obtained in monkey C were related to global
luminance changes caused by stimulus reflection.
Data analysis
SACCADE DETECTION. Eye velocity was determined by convolving eye position records with a Gaussian filter kernel (SD of 4 ms = cutoff frequency of 49 Hz) and then a differencing operator. Fixational saccades were identified as deflections during which eye speed exceeded 6°/s for at least eight consecutive milliseconds. Pairs of deflections satisfying this criterion but separated by <30 ms were considered a single movement. This algorithm reliably detected small-amplitude saccades, which have correspondingly low velocities, but may have detected some nonsaccadic eye movements as well.
As described in RESULTS, most of the detected movements appeared
to be saccades by standard criteria, but an appreciable fraction had looping
trajectories for which the start and end points were nearly coincident. Such
trajectories are consistent with blinks
(Bair and O'Keefe 1998;
Collewijn et al. 1985;
Goossens and Van Opstal 2000).
We did not measure the position of the eyelids and therefore do not know how
much they moved during the eye movements we studied. Several lines of
evidence, however, suggest that few if any of the movements we analyzed were
blinks. First, during a blink, the eye is typically displaced by >1°
with a peak speed >50°/s (Bair and
O'Keefe 1998; Collewijn et al.
1985; Goossens and Van Opstal
2000). Such movements would have resulted in fixation breaks in
our task, and none of the movements we studied fell within this range. Second,
fixating monkeys performing other tasks rarely make eye movements consistent
with blinks (Bair and O'Keefe
1998), and we failed to observe, via video monitoring, frequent
blinking during performance of our task. Nonetheless, monkey C made
approximately one small amplitude looping eye movement per second when the
stimulus was present and also when it was absent. Third, we analyzed
separately movements with straight and looping trajectories but were unable to
find convincing differences between them with respect to their stimulus
dependence. We therefore include all detected movements in the analyses that
follow and refer to them as "saccades" for ease of exposition, but
note that some of them may have been high-velocity, nonsaccadic movements. A
typical eye position record, with saccade detections indicated, appears in
Fig. 2.
|
To estimate the noise in our eye position measurements, we calculated the SD of eye position during the 50 ms after movement offset, during which the saccadic system may be refractory. Changes in eye position during this period reflect physiological noise including slow drifts and tremors as well as electrical noise inherent to our measurement system. Averaged across movements, horizontal and vertical channels, and monkeys, the SD was 0.015°, indicating relatively stable eye position. Assuming Gaussian distributed noise that is independent across samples, the probability of the eye speed exceeding our 6°/s threshold by chance is 3 x 10–5. This implies a false alarm probability of <1% during each second of recording.
SACCADE-TRIGGERED AVERAGE. Previous studies have employed the
reverse-correlation method to study the relationship between sensory stimuli
and neuronal or psychophysical responses (e.g.,
Ahumada 1996;
Marmarelis and Marmarelis
1978). We used it to relate our stimulus to the occurrence of
fixational saccades. For each saccade, the sequence of 20 stimulus frames (200
ms) preceding saccade initiation were extracted and represented numerically as
the intensities of the three monitor phosphors. The saccade-triggered average
stimulus (STA) was calculated as the intensity of each phosphor at each of the
20 frames leading up to the saccade, averaged across saccades. Saccade
initiations were assigned to the beginning of each frame: initiations
occurring from 0 to 9 ms after a screen refresh were considered to be
coincident with the refresh for the purpose of computing the STA.
The stochastic nature of our stimulus simplified hypothesis testing on the
STA. By construction, the intensity of each phosphor in a given stimulus frame
is an approximately Gaussian random variable with mean µphosp
and variance 
2. The average of n randomly selected
intensities, for a given phosphor, thus has a Gaussian distribution with
variance 2/n. Under the assumption that the
stimulus sequence does not influence the probability of saccade initiation,
the STA is simply the average of many randomly selected stimulus sequences. In
this case, every point in the STA has a Gaussian distribution with mean 0 and
variance 2/n (after having subtracted off the mean
intensity values, µphosp). Departures from this distribution
indicate a relationship between the stimulus sequence and saccade initiations.
We express STAs in units of SEs to correct for the fact that its variance
depends on n.
|
|
RESULTS |
|---|
|
Saccades that caused the eye to leave the fixation window were excluded from all analyses. Saccades obtained during nonstimulated trials were likewise excluded except where stated otherwise. Monkey C made 118,704 saccades during 46,976 s of accumulated stimulated trials, resulting in an average frequency of 2.5 saccades/s. Monkey T made 201,428 saccades in 89,429 s, or 2.3 saccades/s.
Distributions of saccade directions differed between monkeys, as shown in
Fig. 3, A and
B. Monkey C's saccades were distributed broadly
but biased downward. Monkey T's saccades were usually directed
downward, less frequently upward, and rarely horizontally. Saccade directions
were not obviously related to the stimulus location: the stimulus was
presented to the left for monkey C and to the right for monkey
T, as shown Fig. 3 A and
B, 
. Saccades in these directions were not
particularly common.
|
Distributions of saccade amplitudes also differed between monkeys as shown
in Fig. 1, C and
D. The largest saccade allowed, theoretically, was
(corner to opposite corner of the fixation window).
Empirically, however, amplitudes tended to be well below this upper bound:
0.14 ± 0.08° and 0.27 ± 0.13° (means ± SD) for
monkeys C and T, respectively. Peak eye speed covaried with
movement amplitude for both monkeys as shown in
Fig. 3, E and
F. Most movements we studied belonged to the "main
sequence" of saccades: their amplitudes and speeds lay on a line passing
through the origin. Interestingly however, monkey C made many small
amplitude movements with looping trajectories and velocities higher than
expected from the main sequence: 53% of monkey C's movements lay
above the diagonal line in Fig.
3E (only 5% of monkey T's movements were in this
range). The first eyeposition deflection in
Fig. 2 is a small movement with
a looping trajectory. Saccade amplitude covaried with direction for both
monkeys. Figure 3, E and
F, shows mean saccade amplitude as a function of saccade
direction. Linear-circular correlation coefficients
(Batschelet 1981) for
monkey C (0.048) and monkey T (0.031) were highly
significant (P < 0.0001). Interestingly, directions of high
saccade frequency tended to be directions of high saccade amplitude (compare
Fig. 3, A and B with
G and H).
Luminance transients elicit saccades
Irwin et al. (2000) showed
that luminance transients can elicit reflexive saccades in human subjects,
suggesting that some of the saccades that we recorded may have been related to
luminance changes in the stimulus. To test this hypothesis, we extracted the
sequence of stimulus frames preceding each saccade and, by averaging phosphor
intensities, derived the average sequence of frames preceding a saccade. As
shown in Fig. 4, these
saccade-triggered averages (STAs) were surprisingly consistent between
monkeys: on average, the stimulus that preceded a saccade was a small
decrease, followed by a larger increase, in phosphor intensity.
|
The three monitor phosphors differed in their ability to elicit a saccade. On average, increments in the green phosphor were most effective, increments in the blue phosphor were less effective, and the red phosphor did not appear to drive saccades at all. This is roughly, but not exactly, the pattern expected if the saccades were driven by the luminance of the stimulus. We return to this issue in the DISCUSSION.
Stimulus-evoked saccades had remarkably short latencies. STAs peaked
70 ms before saccade initiation for both monkeys. This indicates that the
entire chain of events, from visual transduction to contraction of the
extraocular muscles, is completed within 70–80 ms. In fact, points in
the STA lie outside the 99% confidence interval even closer in time to saccade
initiation, suggesting that the minimum latency may be slightly shorter.
Directions of stimulus-evoked saccades
Our monkeys made saccades of many directions (Fig. 3, A and B). We considered the possibility that luminance transients in our stimulus attracted saccades and that saccades in other directions were spontaneous. We tested this hypothesis in two ways, neither of which supported the hypothesis.
In the first analysis, we binned saccades by direction, calculated STAs for
saccades in each bin, and quantified intensity transients in each STA with an
STA index. Only green and blue phosphors were considered in this analysis
because the red phosphor was ineffective at driving saccades (see
Fig. 4). The STA index is
defined as the average difference between the phosphor intensities from 60 to
90 ms preceding each saccade and from 100 to 120 ms preceding each saccade.
This index will be positive for STAs exhibiting a trough near 110 ms and a
peak near 70 ms (like those shown in Fig.
4), will be negative for STAs with trough and peak reversed, and
will be close to zero for STAs that are flat or random. Under the null
hypothesis, this index has a Gaussian distribution with a mean of 0 and a
variance of 2/(14n). We express STA indices in
units of standard errors to correct for the fact that its variance depends on
n. Importantly, positive and negative indices are equally likely
under the null hypothesis.
Figure 5, A and B, shows the STA index as a function of saccade direction. Surprisingly, the index was uniformly positive, indicating that saccades in all directions were preceded, on average, by a decrease and then an increase in stimulus luminance. Saccades toward the stimulus (to the left for monkey C and to the right for monkey T) did not lead to particularly large indices. Luminance transients therefore evoke saccades of many directions not just toward the stimulus.
|
Additionally, we investigated the stimulus-dependence of saccade directions by measuring fixational eye movements made during interleaved stimulated and nonstimulated trials. Polar frequency histograms of saccade directions appear in Fig. 5, C and D, for saccades made in the presence (black curve) and the absence (gray curve) of the stimulus. Although the histograms are quite similar visually, the distribution of saccade directions differed significantly between stimulus conditions for both monkeys (Mardia-Watson-Wheeler tests, P < 0.001). Counterintuitively, saccade directions were biased weakly away from the stimulus for both monkeys, by 1.3° for monkey C and by 6.9° for monkey T. This result suggests that the stimulus did not attract fixational saccades but rather repelled them slightly.
Amplitudes of stimulus-evoked saccades
We considered the possibility that luminance transients evoked saccades of only a particular range of amplitudes. To test this hypothesis, we binned saccades by amplitude and calculated an STA index for saccades in each bin. The results of this analysis appear in Fig. 6, A and B. STA indices for both monkeys were positive and of similar magnitude across a broad range of amplitudes, indicating that luminance transients drove saccades of many amplitudes similarly.
|
We also compared saccade amplitudes in the presence and absence of the stimulus. Frequency histograms for stimulated (black) and nonstimulated (gray) conditions appear in Fig. 6, C and D. For monkey C, the stimulus decreased the mean amplitude by 0.007°. This effect was reversed, however, for monkey T for whom the stimulus increased the mean amplitude by 0.018°. Both changes were significant (t-test, P < 0.0001). We thus conclude that peripheral visual stimulation affects the amplitudes of fixational saccades significantly but inconsistently.
|
|
DISCUSSION |
|---|
|
70 ms. Saccades varied idiosyncratically between monkeys in amplitudes
and direction. The average stimulus preceding a saccade, however, was
remarkably consistent: saccades followed a decrease, then an increase, in
phosphor intensity. Saccades were biased weakly away from the stimulus. Spectral sensitivity
Saccade initiations were related most closely to intensity changes in the green phosphor. This is what one would expect if saccades were triggered by changes in stimulus luminance: although each phosphor in our stimulus varied over a similar radiometric range, they varied over different luminance ranges due to their different emission spectra. The green phosphor underwent the greatest luminance changes, and it drove saccades effectively; the red and the blue phosphors underwent smaller luminance changes and drove saccades much less effectively. If saccades were driven purely by luminance, however, the red phosphor would have been more effective than the blue. This was not the case, so we infer that the mechanism that drove saccades in our experiment is relatively more sensitive to short wavelength light (i.e., the light emitted by the blue phosphor).
Enhanced sensitivity to short wavelength light, relative to luminance,
could arise from a number of sources. First, the stimulus was presented in the
peripheral visual field, where lack of macular pigment increases
psychophysical sensitivity to short wavelength light
(Wyszecki and Stiles 1982).
Second, macaque monkeys may be more sensitive to short wavelength light than
humans are (DeValois et al.
1974). Consistent with this idea, we find that many macaque V1
neurons exhibit similarly enhanced sensitivity at short wavelengths relative
to luminance (G. D. Horwitz, E. J. Chichilnisky, and T. D. Albright,
unpublished observations).
The saccades we observed may have been driven by multiple mechanisms with varied spectral sensitivities. In this case, the STA would reflect the average sensitivity of the underlying mechanisms but not necessarily the sensitivity of any single one. Likewise, saccades may have been driven by different mechanisms at different latencies. For instance, our data are consistent with a single mechanism than drove saccades in response to the sequential presentation of a luminance decrement followed by an increment or alternatively, two independent mechanisms: one that drove short-latency saccades in response to luminance increments and another that drove saccades at a longer latency in response to luminance decrements. Our analysis method does not allow us to determine how many spectrally or temporally distinct mechanisms drove saccades in our experiment.
Saccades in our experiment were driven primarily by luminance changes on
average, but express saccades, which have a similar latency, can be made to
both luminant and isoluminant targets
(McPeek and Schiller 1994;
Weber et al. 1991). Despite
this apparent discrepancy, a common mechanism may underlie the saccades we
studied and express saccades. First, if multiple mechanisms contributed to the
saccades we studied, those sensitive to pure color modulations may have been
hidden in the STA. This would be expected if saccades were driven equally well
by opponent colors (which would cancel in the STA) or if our stimulus
activated luminance mechanisms more effectively than chromatic mechanisms.
Second, we found that fixational saccades were more readily evoked by short
wavelength light than expected from luminance. Isoluminant modulations, which
by definition do not activate a luminance mechanism, might therefore still
activate the mechanism responsible for driving fixational saccades, if
weakly.
Comparison with previous work
Tse et al. (2002) looked
for, and failed to reveal, a relationship between fixational eye movements and
peripheral luminance transients. A variety of methodological differences
between our study and that of Tse et al. could account for the difference in
result. First, Tse et al. tested human subjects, whereas we tested monkeys.
Monkeys may be less able to suppress reflexive saccades than humans (but see
Amador et al. 1998;
Bell et al. 2000;
Steinman et al. 1973). Second,
subjects in the Tse et al. study performed a demanding novelty detection task
during data collection and were instructed explicitly to ignore the peripheral
flash. Our monkeys fixated without performing any other task; they were
therefore free to attend to the stimulus and may have done so. Third, we
analyzed saccades specifically, whereas Tse et al. considered only average eye
position during periods of nominal fixation. We found that saccades induced by
luminance transients were broadly distributed in direction and amplitude. If
saccades in the study of Tse et al. were similarly distributed, it would be
therefore unsurprising that stimulus position was not related clearly to mean
eye position.
Saccade frequencies in our study were somewhat higher than in previous
studies of fixating monkeys (Bair and
O'Keefe 1998; Leopold and
Logothetis 1998). This discrepancy is presumably due in part to
differences in saccade detection algorithms: we set a fairly low velocity
threshold and included eye movements with strongly curved trajectories,
whereas previous studies have used stricter criteria. Details of our
behavioral task including the display luminance and the presence of a salient
peripheral stimulus may also have increased saccade frequencies.
Directions of stimulus-evoked fixational saccades
The amplitudes of saccades evoked by visual onsets or by electrical
stimulation are diminished during active fixation
(Sparks and Mays 1983;
Weber et al. 1993). This
raises the possibility that the saccades we observed were directed toward the
stimulus but were hypometric as a result of fixation and therefore failed to
leave the fixation window. This was not the case. Luminance transients
preceded saccades in many directions, including away from the stimulus.
Furthermore, presentation of the stimulus actually biased saccades weakly
toward the opposite hemifield. We conclude that, under the conditions of our
experiment, peripheral luminance transients increase the probability of a
saccade and that these saccades are not directed toward the stimulus.
A priori, one might expect peripheral luminance transients to attract
saccades. Such a reflex is of obvious utility, it has been documented in
previous studies (e.g., Theeuwes et al.
1999), and candidate neural mechanisms are becoming understood
(see Isa 2002 for a review).
Details of our behavioral task may have prevented the saccades we studied from
being directed toward the stimulus. Our fixation window, for example, was
sufficiently small that even a few small co-directional saccades, without
intervening compensatory eye movements, would have resulted in a fixation
break and thus a penalty for the monkey. Our monkeys may therefore have
adopted a strategy to compensate for the reflex to acquire the stimulus.
Preparing small amplitude saccades away from the stimulus, for instance, might
have prolonged fixation durations. Enlarging the fixation window might reveal
a relationship between the stimulus location and saccade direction.
Stimulus-evoked saccades may have been directed toward the fixation point. Two lines of reasoning lend credibility to this notion: first, peripheral luminance transients may have enhanced the contrast of the black fixation point by raising the mean luminance of the background. The fixation point may have then provided a particularly salient saccade target. Second, stimulus-evoked saccades may have been directed toward the weighted average position of the fixation point and the stimulus with very little weight assigned to the stimulus. In this case, stimulus-evoked saccades would be expected to land near the fixation point. Unfortunately, our experiment does not permit us to test these hypotheses rigorously: slow drifts in the eye-tracking system, combined with uncertainty in mean fixation position relative to the fixation point, prevent us from classifying decisively saccades as centripetal or centrifugal.
Neural mechanisms
The superior colliculus may participate in generating the saccades we
studied. First, saccade latencies in our experiment were extremely short,
indicating a relatively direct pathway from retina to extraocular musculature.
By comparison, voluntary visually guided saccades typically have latencies of
120 ms. The colliculus receives input from the retina and visual cortex,
and it projects to oculomotor nuclei in the brain stem, appropriate for
driving short-latency saccades. Second, superficial layer SC neurons, like the
saccades we observed, are tuned roughly for luminance
(Marrocco and Li 1977). We do
not know whether the deviation from luminance tuning we observed is reflected
in the spectral sensitivity of collicular neurons. Third, collicular ablation
eliminates express saccades, which have latencies similar to those we measured
and may therefore derive from a common neural circuit
(Schiller et al. 1980). A
testable extension of this idea is that the short latencies we observed are
related to the highly predictable location of our stimulus: express saccades
occur more frequently when target position is predictable than when it is not
(Pare and Munoz 1996).
In apparent contradiction to our findings, Reingold and Stampe
(2002) showed that a
peripheral luminance increment can inhibit a visually guided saccade with a
latency of 70 ms. In their study, human subjects were instructed to
execute 4° horizontal saccades while luminance flashes were presented
either above or below the fixation point. Their study differed from ours in a
number of respects including subject species, task demands, and stimulus
parameters. Any of these methodological differences could contribute to the
difference in result.
On the other hand, a common mechanism may underlie both results. Reingold
and Stampe proposed that collicular neurons in whose response field a flash
occurs may inhibit other collicular neurons that mediate the intended
behavior. Saccades in their task required the activity of saccade-related
burst neurons at the 4° site in the collicular map
(Robinson 1972). The
peripheral flash might have inhibited these neurons. Monkeys in our experiment
were required only to fixate, which presumably requires the balanced activity
of "fixation neurons" at the rostral pole of the colliculus
(Munoz and Wurtz 1993). If
fixation neurons are inhibited by a peripheral flash, one might expect
fixation to be impaired, as we observed. Support for this idea comes from the
existence of lateral inhibition within the colliculus and the apparent
continuum between fixation neurons and those involved in saccade preparation
(Munoz and Istvan 1998;
Munoz and Wurtz 1995).
Luminance flashes may therefore disrupt saccades and fixation
nonspecifically.
|
|
DISCLOSURES |
|---|
|
|
|
ACKNOWLEDGMENTS |
|---|
|
|
|
FOOTNOTES |
|---|
Address for reprint requests: Gregory D. Horwitz, Vision Center Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd., La Jolla, CA 92037 (E–mail: horwitz{at}salk.edu).
|
|
REFERENCES |
|---|
|
Amador N,
Schlag-Rey M, and Schlag J. Primate antisaccades. I. Behavioral
characteristics. J Neurophysiol
80: 1775–1786,
1998.
Bair W and O'Keefe LP. The influence of fixational eye movements on the response of neurons in area MT of the macaque. Vis Neurosci 15: 779–786, 1998.[Web of Science][Medline]
Batschelet E. Circular Statistics in Biology. New York: Academic, 1981.
Bell AH,
Everling S, and Munoz DP. Influence of stimulus eccentricity and direction
on characteristics of pro- and antisaccades in non-human primates.
J Neurophysiol 84:
2595–2604, 2000.
Chichilnisky EJ and Wandel BA. Trichromatic opponent color classification. Vision Res 39: 3444–3458, 1999.[Web of Science][Medline]
Collewijn H,
van der Steen J, and Steinman RM. Human eye movements associated with
blinks and prolonged eyelid closure. J Neurophysiol
54: 11–27,
1985.
Corbetta M, Akbudak E, Conturo TE, Snyder AZ, Ollinger JM, Drury HA, Linenweber MR, Petersen SE, Raichle ME, Van Essen DC, and Shulman GL. A common network of functional areas for attention and eye movements. Neuron 21: 761–773, 1998.[Web of Science][Medline]
DeValois R, Morgan H, Polson M, Mead W, and Hull E. Psychophysical studies of monkey vision. I. Macaque luminosity and color vision tests. Vision Res 14: 53–67, 1974.[Web of Science][Medline]
Goossens HH and
Van Opstal AJ. Blink-perturbed saccades in monkey. I. Behavioral analysis.
J Neurophysiol 83:
3411–3429, 2000.
Irwin D, Colcombe A, Kramer A, and Hahn S. Attentional and oculomotor capture by onset, luminance and color singletons. Vision Res 40: 1443–1458, 2000.[Web of Science][Medline]
Isa T. Intrinsic processing in the mammalian superior colliculus. Curr Opin Neurobiol 12: 668–677, 2002.[Web of Science][Medline]
Judge SJ, Richmond BJ, and Chu FC. Implantation of magnetic search coils for measurement of eye position: an improved method. Vision Res 20: 535–538, 1980.[Web of Science][Medline]
Kustov AA and Robinson DL. Shared neural control of attentional shifts and eye movements. Nature 384: 74–77, 1996.[Medline]
Leopold DA and Logothetis NK. Microsaccades differentially modulate neural activity in the striate and extrastriate visual cortex. Exp Brain Res 123: 341–345, 1998.[Web of Science][Medline]
Marmarelis P and Marmarelis V. Analysis of Physiological Systems: The White Noise Approach. New York: Plenum, 1978.
Marrocco RT and
Li RH. Monkey superior colliculus: properties of single cells and their
afferent inputs. J Neurophysiol
40: 844–860,
1977.
McPeek RM and Schiller PH. The effects of visual scene composition on the latency of saccadic eye movements of the rhesus monkey. Vision Res 34: 2293–2305, 1994.[Web of Science][Medline]
Munoz DP and
Istvan PJ. Lateral inhibitory interactions in the intermediate layers of
the monkey superior colliculus. J Neurophysiol
79: 1193–1209,
1998.
Munoz DP and
Wurtz RH. Fixation cells in the monkey superior colliculus. I.
Characteristics of cell discharge. J Neurophysiol
70: 559–575,
1993.
Munoz DP and
Wurtz RH. Saccade-related activity in monkey superior colliculus. I.
Characteristics of burst and buildup cells. J
Neurophysiol 73:
2313–2333, 1995.
Pare M and
Munoz DP. Saccadic reaction time in the monkey: advanced preparation of
oculomotor programs is primarily responsible for express saccade occurrence.
J Neurophysiol 76:
3666–3681, 1996.
Posner MI, Snyder CRR, and Davidson BJ. Attention and the detection of signals. J Exp Psychol Gen 109: 160–174, 1980.[Web of Science][Medline]
Reingold EM and Stampe DM. Saccadic inhibition in voluntary and reflexive saccades. J Cogn Neurosci 14: 371–388, 2002.[Web of Science][Medline]
Robinson DA. Eye movements evoked by collicular stimulation in the alert monkey. Vision Res 12: 1795–1807, 1972.[Web of Science][Medline]
Schiller P,
True S, and Conway J. Deficits in eye movements following frontal
eye-field and superior colliculus ablations. J
Neurophysiol 44:
1175–1189, 1980.
Sparks DL and
Mays LE. Spatial localization of saccade targets. I. Compensation for
stimulation-induced perturbations in eye position. J
Neurophysiol 49:
45–63, 1983.
Steinman RM,
Haddad GM, Skavenski AA, and Wyman D. Miniature eye movement.
Science 181:
810–819, 1973.
Theeuwes J, Kramer A, Hahn S, and Irwin D. Our eyes do not always go where we want them to go: capture of the eyes by new objects. Psychol Sci 9: 379–385, 1998.[Web of Science]
Theeuwes J, Kramer AF, Hahn S, Irwin DE, and Zelinsky GJ. Influence of attentional capture on oculomotor control. J Exp Psychol Hum Percept Perform 25: 1595–1608, 1999.[Web of Science][Medline]
Tse PU, Sheinberg DL, and Logothetis NK. Fixational eye movements are not affected by abrupt onsets that capture attention. Vision Res 42: 1663–1669, 2002.[Web of Science][Medline]
Weber H, Fischer B, Bach M, and Aiple F. Occurrence of express saccades under isoluminance and low contrast luminance conditions. Vis Neurosci 7: 505–510, 1991.[Web of Science][Medline]
Weber H, Latanov A, and Fischer B. Context dependent amplitude modulations of express and regular saccades in man and monkey. Exp Brain Res 93: 335–344, 1993.[Web of Science][Medline]
Wyszecki G and Stiles W. Color Science: Concepts and Methods, Quantitative Data and Formulae. New York: Wiley, 1982.
This article has been cited by other articles:
|
|
 |
|
  G. D. Horwitz, E. J. Chichilnisky, and T. D. Albright Cone Inputs to Simple and Complex Cells in V1 of Awake Macaque J Neurophysiol, April 1, 2007; 97(4): 3070 - 3081. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
TOP
ABSTRACT
INTRODUCTION
) were placed in
several locations to the left of the fixation point (
) for monkey
C, and in 1 location to the right of the fixation point for monkey
T. The screen subtended 31 x 23° (outer border). Monkeys were
required to maintain fixation within a 1 x 1° electronically defined
window around the fixation point (- - -).
, see
METHODS). - - -, the 99% confidence interval. On average, a saccade
is preceded by a decrease, followed by an increase, in phosphor intensity. The
green phosphor undergoes the clearest fluctuation, which peaks 70 ms before
the saccade.
