The presaccadic cortical negativity prior to self-paced saccades with and without visual guidance

The presaccadic negativity (PSN) of the scalp EEG potential prior to self-initiated saccades aimed either at a visual target or at the remembered position of that target in total darkness was analysed in 10 normal subjects. Under both conditions a PSN with a negligible EOG contamination was found, showing 4 characteristics: (1) In both conditions, the PSN maximum is localized at the vertex, probably containing the activity of the supplementary motor area. (2) At an electrode placed over the frontal eye field (FEF) contralateral to the saccade direction, there is a temporary, circumscribed maximum prior to saccades to the visual target, thus probably reflecting activity of the FEF. (3) Prior to saccades to the visual target, there is a statistically significant interhemispheric difference of the PSN over the parietal cortex with a larger amplitude over the hemisphere contralateral to the saccade direction; this might be attributed to directed visual attention. (4) Prior to saccades without visual guidance in darkness there is a statistically significant interhemispheric difference of the PSN over the frontal cortex with a larger amplitude over the hemisphere contralateral to the saccade direction. The amplitude of the PSN decreased in the course of the experiment, probably due to psychological factors such as attention and motivation. Our results suggest that the PSN is a readiness potential preceding voluntary saccades, containing activity related both to unspecific psychological processes and to specific movement preparation in the frontal and parietal ocular motor areas.     

Presaccadic attention allocation and express saccades

Express saccades are visually-guided saccades that are characterized by an extremely short latency of about 100 ms. The present experiments tested the hypothesis that a disengagement of visual attention is necessary for the generation of express saccades. All subjects produced large numbers of express saccades in the gap paradigm, in which the fixation stimulus is removed 200 ms before target onset (Exp. 1), but not in the overlap paradigm, in which the fixation stimulus remained on during the entire trial (Exp. 2). By means of peripheral cues (Exps. 3-5) and central cues (Exps. 6-7), visual attention was directed at the target location for the saccade before the actual appearance of the saccade target. In all experiments, the location cues facilitated rather than abolished express saccades. The generation of express saccades was facilitated even when the currently fixated visual stimulus was not removed before target onset (fixation-overlap; Exps. 5-7). The results are explained by the hypothesis that a disengagement of a separate fixation system is necessary for the generation of express saccades, a hypothesis that is in line with current neurobiological findings.     

Discharge properties of Purkinje cells in the oculomotor vermis during visually guided saccades in the macaque monkey

1. We previously described discharge properties of cerebellar output cells in the fastigial nucleus during ipsilateral and contralateral saccades. Fastigial cells exhibited unique responses depending on the direction of saccades and were involved in execution of accurate targeting saccades. Purkinje cells in the oculomotor vermis (lobules VIc and VII) are thought to modulate these discharges of fastigial cells. In this study we reexamine discharge properties of Purkinje cells on the basis of this hypothesis. 2. Initially we physiologically identified the right and left sides of the oculomotor vermis. Saccade-related discharges of 79 Purkinje cells were recorded from both sides of the vermis during visually guided saccades toward the sides ipsilateral and contralateral to the recording side in two trained macaque monkeys. To clarify the correlation of Purkinje cell discharge with burst activities in the fastigial nucleus during saccadic eye movements, we analyzed our data by employing methods used in the study of fastigial neurons. 3. Among the 79 cells, 56 (71%) showed burst discharges during saccades (saccadic burst cells). Of the 56 cells, 29 exhibited a peak of burst discharges in both the contralateral and ipsilateral directions (bidirectional cells). The remaining 27 saccadic burst cells showed a peak of burst discharges during either contralateral or ipsilateral saccades (unidirectional cells). Among the 79 cells, 14 (18%) exhibited a pause of discharges during contralateral saccades (pause cells). Among the 79 cells, 9 (11%) showed burst discharge during contralateral saccades followed by tonic discharge that was correlated with eye position (burst tonic cells). 4. The timing of bursts in bidirectional cells with respect to saccade onset was dependent on the direction of saccade. During ipsilateral saccades, Purkinje cells exhibited a long lead burst that built up gradually, peaked near the onset of the saccade, and terminated sharply near midsaccade. The mean lead time relative to saccade onset was 29.3 +/- 24.5 (SD) ms. During contralateral saccades, Purkinje cells exhibited a short lead/late burst that built up sharply, peaked near midsaccade, and terminated gradually after the end of the saccade. The mean lead time relative to saccade onset was 10.7 +/- 20.8 ms. The burst onset time during contralateral saccades and the burst offset time during ipsilateral saccades preceded the saccade offset time by about the same interval regardless of the saccade amplitude. 5. In pause cells the pause preceded saccade onset by 17.5 +/- 10.6 ms. The duration of the pause was not correlated with the duration of saccades. There was little trial-to-trial variability in the onset time of the pause with respect to the onset of saccades, whereas there was large trial-to-trial variability in the offset time of the pause with respect to the offset of saccades. In addition, the mean onset time of the pause for each cell had a relatively narrow distribution. 6. The burst lead time of burst tonic cells relative to saccade onset was 9.5 +/- 3.9 ms. The tonic discharge rate of burst tonic cells was a nonlinear function of eye position. The regression of each cell was fit to two lines. The regression coefficient ranged from 0.95 to 0.99 (mean = 0.97). 7. Axons of Purkinje cells in the oculomotor vermis are thought to project exclusively to saccadic burst cells in the fastigial oculomotor region (FOR), which is located in the caudal portion of the fastigial nucleus. Our previous studies indicated that FOR cells provide temporal signals for controlling targeting saccades. The present results suggest that Purkinje cells in the oculomotor vermis modify the temporal signals of FOR cells for saccades in different directions and amplitudes. The modification of FOR cell activity by Purkinje cells is thought to be essential for the function of the cerebellum in the control of saccadic eye movements.     

Bilateral interactions in saccade programming. A saccade-latency study

Subjects were required to make a saccade to a target appearing randomly 4 degree to the left or right of the current fixation position (1280 trials per experiment). Location cues were used to direct visual attention and start saccade preparation to one of the two locations before target onset. When the cue indicated the target location (valid trials), the generation of express saccades (visually guided saccades with latencies around 100 ms) was strongly facilitated. When the opposite location was cued (invalid trials), express saccades were abolished and replaced by a population of mainly fast-regular saccades (latencies around 150 ms). This was found with a peripheral cue independently of whether the fixation point was removed before target onset (gap condition; experiment 1) or remained on throughout the trial (overlap condition; experiment 2). The same pattern also was observed with a central cue that did not involve any visual stimulation at a peripheral location (experiment 3). In the case where the primary saccade was executed in response to the cue and the target appeared at the opposite location, continuous amplitude transition functions were observed: starting at about 60-70 ms from target onset onward, the amplitude of the cue-elicited saccades continuously decreased from 4 degree to values below 1 degree. The results are explained by a fixation-gating model, according to which the antagonism between fixation and saccade activity gives rise to multimodal distributions of saccade latencies. It is argued that allocation of visual attention and saccade preparation to one location entails a successive disengagement of the fixation system controlling saccade preparation within the hemifield to which the saccade is prepared and a partial engagement of the opposite fixation system.     

Visualization of the information flow through human oculomotor cortical regions by transcranial magnetic stimulation

We investigated the topography of human cortical activation during an antisaccade task by focal transcranial magnetic stimulation (TMS). We used a figure-eight shaped coil, with the stimulus intensity set just above the threshold for activation of the hand motor areas but weak enough not to elicit blinks. TMS was delivered at various time intervals (80, 100, and 120 ms) after target presentation over various sites on the scalp while the subjects performed the antisaccade task. It was possible to elicit a mild but significant delay in saccade onset over 1) the frontal regions (a region 2-4 cm anterior and 2-4 cm lateral to hand motor area) and 2) posterior parietal regions (6-8 cm posterior and 0-4 cm lateral to hand motor area) regardless of which hemisphere was stimulated. The frontal regions were assumed to correspond to a cortical region including the frontal eye fields (FEFs), whereas the parietal regions were assumed to represent a wide region that includes the posterior parietal cortices (PPCs). The regions inducing the delay shifted from the posterior parietal regions at an earlier interval (80 ms) to the frontal regions at a later interval (100 ms), which suggested an information flow from posterior to anterior cortical regions during the presaccadic period. At 120 ms, the effect of TMS over the frontal regions still persisted but was greatly diminished. Erroneous prosaccades to the presented target were elicited over a wide cortical region including the frontal and posterior parietal regions, which again showed a forward shift with time. However, the distribution of effective regions exhibited a clear contralateral predominance in terms of saccade direction. Our technique provides a useful method not only for detecting the topography of cortical regions active during saccadic eye movement, but also for constructing a physiological map to visualize the temporal evolution of functional activities in the relevant cortical regions.     

The transcriptional effects and DNA-binding specificities of 17beta-estradiol after dimethyldioxirane activation

We investigated the spatio-temporal brain activity on the time scale of several milliseconds related to the mental rotation task requiring judgements of hand orientation, using a whole-cortex MEG (magnetoencephalography) system. Neuronal activity in the visual cortex was observed approximately 100-200 ms from stimulus onset, and that in inferior parietal lobe followed (after 200 ms). Both of these activities showed a contralateral dominance to visual stimulus hemifield. Premotor activity started later than the inferior parietal lobe activity, and these activities partially overlapped. Activity in primary motor and/or motosensory areas was observed in some subjects. The whole-cortex neuromagnetic measurements provided the time course of activity in the human brain associated with the implicit motor imagery: visual cortex-->inferior parietal lobe<-->premotor cortex. This process is considered to be the transformation process of retinotopic locations into a body-centered reference frame necessary for the mental rotation task.     

Reaction times of vertical prosaccades and antisaccades in gap and overlap tasks

Horizontal saccadic reaction times (SRTs) have been extensively studied over the past 3 decades, concentrating on such topics as the gap effect, express saccades, training effects, and the role of fixation and attention. This study investigates some of these topics with regard to vertical saccades. The reaction times of vertical saccades of 13 subjects were measured using the gap and the overlap paradigms in the prosaccade task (saccade to the stimulus) and the antisaccade task (saccade in the direction opposite to the stimulus). In the gap paradigm, the initial fixation point (FP) was extinguished 200 ms before stimulus onset, while, in the overlap paradigm, the FP remained on during stimulus presentation. With the prosaccade overlap task, it was found that most subjects (10/13)-whether they were previously trained making horizontal saccades or naive-had significantly faster upward saccades compared with their downward saccades. One subject was faster in the downward direction and two were symmetrical. The introduction of the gap reduced the reaction times of the prosaccades, and express saccades were obtained in some naive and most trained subjects. This gap effect was larger for saccades made to the downward target. The strength of the updown asymmetry was more pronounced in the overlap as compared to the gap paradigm. With the antisaccade task, up-down asymmetries were much reduced. Express antisaccades were absent even with the gap paradigm, but reaction times were reduced as compared to the antisaccade overlap paradigm. There was a slight tendency for a larger gap effect of downward saccades. All subjects produced a certain number of erratic prosaccades in the antitasks, more with the gap than with the overlap paradigm. There was a significantly larger gap effect for the erratic prosaccades made to the downward, as compared to the upward, target, due to increased downward SRTs in the overlap paradigm. Three subjects trained in both the horizontal and the vertical direction showed faster SRTs and more express saccades in the horizontal directions as compared to the vertical. It is concluded that different parts of the visual field are differently organized with both directional and nondirectional components in saccade preparation.     

Lateral inhibitory interactions in the intermediate layers of the monkey superior colliculus

The intermediate layers of the monkey superior colliculus (SC) contain neurons the discharges of which are modulated by visual fixation and saccadic eye movements. Fixation neurons, located in the rostral pole of the SC, discharge action potentials tonically during visual fixation and pause for most saccades. Saccade neurons, located throughout the remainder of the intermediate layers of the SC, discharge action potentials for saccades to a restricted region of the visual field. We defined the fixation zone as that region of the rostral SC containing fixation neurons and the saccade zone as the remainder of the SC. It recently has been hypothesized that a network of local inhibitory interneurons may help shape the reciprocal discharge pattern of fixation and saccade neurons. To test this hypothesis, we combined extracellular recording and microstimulation techniques in awake monkeys trained to perform oculomotor paradigms that enabled us to classify collicular fixation and saccade neurons. Microstimulation was used to electrically activate the fixation and saccade zones of the ipsilateral and contralateral SC to test for inhibitory and excitatory inputs onto fixation and saccade neurons. Saccade neurons were inhibited at short latencies following electrical stimulation of either the ipsilateral (1-5 ms) or contralateral (2-7 ms) fixation or saccade zones. Fixation neurons were inhibited 1-4 ms after electrical stimulation of the ipsilateral saccade zone. Stimulation of the contralateral saccade zone led to much weaker inhibition of fixation neurons. Stimulation of the contralateral fixation zone led to short-latency (1-2 ms) excitation of fixation neurons. Only a small percentage of saccade and fixation neurons were activated by the electrical stimulation (latency: 0.5-2.0 ms). These responses were confirmed as either orthodromic or antidromic responses using collision testing. The results suggest that a local network of inhibitory interneurons may help shape not only the reciprocal discharge pattern of fixation and saccade neurons but also permit lateral interactions between all regions of the ipsilateral and contralateral SC. These interactions therefore may be critical for maintaining stable visual fixation, suppressing unwanted saccades, and initiating saccadic eye movements to targets of interest.     

Fixation cells in monkey superior colliculus. I. Characteristics of cell discharge

1. We studied the role of the superior colliculus (SC) in the control of visual fixation by recording from cells in the rostral pole of the SC in awake monkeys that were trained to perform fixation and saccade tasks. 2. We identified a subset of neurons in three monkeys that we refer to as fixation cells. These cells increased their tonic discharge rate when the monkey actively fixated a visible target spot to obtain a reward. This sustained activity persisted when the visual stimulation of the target spot was momentarily removed but the monkey was required to continue fixation. 3. The fixation cells were in the rostral pole of the SC. As the electrode descended through the SC, we encountered visual cells with foveal and parafoveal receptive fields most superficially, saccade-related burst cells with parafoveal movement fields below these visual cells, and fixation cells below the burst cells. From this sequence in depth, the fixation cells appeared to be centered in the deeper reaches of the intermediate layers, and this was confirmed by small marking lesions identified histologically. 4. During saccades, the tonically active fixation cells showed a pause in their rate of discharge. The duration of this pause was correlated to the duration of the saccade. Many cells did not decrease their discharge rate for small-amplitude contraversive saccades. 5. The saccade-related pause in fixation cell discharge always began before the onset of the saccade. The mean time from pause onset to saccade onset for contraversive saccades and ipsiversive saccades was 36.2 and 33.0 ms, respectively. Most fixation cells were reactivated before the end of contraversive saccades. The mean time from saccade terminatioN to pause end was -2.6 ms for contraversive saccades and 9.9 ms for ipsiversive saccades. The end of the saccade-related pause in fixation cell discharge was more tightly correlated to saccade termination, than pause onset was to saccade onset. 6. After the saccade-related pause in discharge, many fixation cells showed an increased discharge rate exceeding that before the pause. This increased postsaccadic discharge rate persisted for several hundred milliseconds. 7. The discharge rate of fixation cells was not consistently altered when the monkey actively fixated targets requiring different orbital positions. 8. Fixation cells discharged during smooth pursuit eye movements as they did during fixation. They maintained a steady tonic discharge during pursuit at different speeds and in different directions, provided the monkey looked at the moving target.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of saccades on the activity of neurons in the cat lateral geniculate nucleus

Effects of saccades on individual neurons in the cat lateral geniculate nucleus (LGN) were examined under two conditions: during spontaneous saccades in the dark and during stimulation by large, uniform flashes delivered at various times during and after rewarded saccades made to small visual targets. In the dark condition, a suppression of activity began 200-300 ms before saccade start, peaked approximately 100 ms before saccade start, and smoothly reversed to a facilitation of activity by saccade end. The facilitation peaked 70-130 ms after saccade end and decayed during the next several hundred milliseconds. The latency of the facilitation was related inversely to saccade velocity, reaching a minimum for saccades with peak velocity >70-80 degrees /s. Effects of saccades on visually evoked activity were remarkably similar: a facilitation began at saccade end and peaked 50-100 ms later. When matched for saccade velocity, the time courses and magnitudes of postsaccadic facilitation for activity in the dark and during visual stimulation were identical. The presaccadic suppression observed in the dark condition was similar for X and Y cells, whereas the postsaccadic facilitation was substantially stronger for X cells, both in the dark and for visually evoked responses. This saccade-related regulation of geniculate transmission appears to be independent of the conditions under which the saccade is evoked or the state of retinal input to the LGN. The change in activity from presaccadic suppression to postsaccadic facilitation amounted to an increase in gain of geniculate transmission of approximately 30%. This may promote rapid central registration of visual inputs by increasing the temporal contrast between activity evoked by an image near the end of a fixation and that evoked by the image immediately after a saccade.     

Human head-free gaze saccades to targets flashed before gaze-pursuit are spatially accurate

Previous studies have shown that accurate saccades can be generated, in the dark, that compensate for movements of the visual axis that result from movements of either the eyes alone or the head alone that intervene between target presentation and saccade onset. We have carried out experiments with human subjects to test whether gaze saccades (gaze = eye-in-space = eye-in-head + head-in-space) can be generated that compensate for smooth pursuit movements of gaze that intervene between target onset and gaze-saccade onset. In both head-unrestrained (head-free) and -restrained (head-fixed) conditions, subjects were asked to make gaze shifts, in the dark, to the remembered location of a briefly flashed target. On most trials, during the memory period, the subjects carried out intervening head-free gaze pursuit or head-fixed ocular pursuit along the horizontal meridian. On the remaining (control) trials, subjects did not carry out intervening pursuit movements during the memory period; this was the classical memory-guided saccade task. We found that the subjects accurately compensated for intervening movements of the visual axis in both the head-free and head-fixed conditions. We conclude that the human gaze-motor system is able to monitor on-line changes in gaze position and add them to initial retinal error, to program spatially accurate gaze saccades.     

When is it best to hear a verb? The effects of the timing and focus of verb models on children''s learning of verbs

Recent neurophysiological studies of the saccadic ocular motor system have lent support to the hypothesis that this system uses a motor error signal in retinotopic coordinates to direct saccades to both visual and auditory targets. With visual targets, the coordinates of the sensory and motor error signals will be identical unless the eyes move between the time of target presentation and the time of saccade onset. However, targets from other modalities must undergo different sensory-motor transformations to access the same motor error map. Because auditory targets are initially localized in head-centered coordinates, analyzing the metrics of saccades from different starting positions allows a determination of whether the coordinates of the motor signals are those of the sensory system. We studied six human subjects who made saccades to visual or auditory targets from a central fixation point or from one at 10 degrees to the right or left of the midline of the head. Although the latencies of saccades to visual targets increased as stimulus eccentricity increased, the latencies of saccades to auditory targets decreased as stimulus eccentricity increased. The longest auditory latencies were for the smallest values of motor error (the difference between target position and fixation eye position) or desired saccade size, regardless of the position of the auditory target relative to the head or the amplitude of the executed saccade. Similarly, differences in initial eye position did not affect the accuracy of saccades of the same desired size. When saccadic error was plotted as a function of motor error, the curves obtained at the different fixation positions overlapped completely. Thus, saccadic programs in the central nervous system compensated for eye position regardless of the modality of the saccade target, supporting the hypothesis that the saccadic ocular motor system uses motor error signals to direct saccades to auditory targets.     

Effects of pre-cues on voluntary and reflexive saccade generation. II. Pro-cues for anti-saccades

The reaction times of saccades (SRT) to a suddenly presented visual stimulus (pro-saccade) can be decreased and a separate mode of express saccades can occur when a gap paradigm is used (i.e. fixation-point offset precedes target onset by 200 ms). A valid peripheral cue, presented briefly (100 ms) before target onset, has been found to facilitate the generation of saccades to the target, thereby increasing the frequency of express saccades and decreasing the mean latency. This facilitation occurs only for cues that correctly indicate the direction of the subsequent target presentation (valid cues). The present study investigates the effects of valid cues on SRTs and error rate in the anti-saccade task (saccades in the direction opposite to the stimulus) by systematically varying the cue lead time (CLT) and using the gap and overlap conditions, i.e. fixation point remains on throughout the trial. For a CLT of 100 ms, both reaction times and error rates were significantly increased. With increasing CLT (200-500 ms), both the reaction times of the anti-saccades and the error rates returned to approximately control level, with CLT more than 200 ms in both the gap and the overlap condition. Additional experiments using non-informative cues in the overlap task showed that the reaction times of correct anti-saccades and the error rate were decreased when cue and stimulus appeared at the same side. Analysis of the erratic pro-saccades revealed that almost all of them were corrected, i.e. they were followed by a second saccade towards the required location. It is found that the correction times were usually very short, with intersaccadic intervals between 0 and 150 ms. We suggest that the orienting mechanism, elicited by a transient peripheral cue, relates to the command and the decision to make a pro- rather than an anti-saccade. The cue elicits pro-orienting towards its position when a pro-saccade is required, and anti-orienting when an anti-saccade is required. The orienting effect is transient and decays with CLTs of more than 200 ms; this result holds for both anti-saccades and pro-saccades. Since subjects reported that they could not prevent the erratic pro-saccades or were often not aware of them, we conclude that this orienting mechanism occurs automatically, beyond voluntary control.     

The interaction of stimulus- and response-related processes measured by event-related lateralizations of the EEG

The present study focused on the relationship between movement- and stimulus-related asymmetries of the electroencephalogram (EEG). In seven tasks the same bilateral stimuli containing asymmetric information were presented but response requirements differed. Three functionally distinct asymmetries were found: (1) an asymmetry over the motor cortex prior to unimanual movements, (2) an asymmetry over the posterior cortex beginning about 20 ms after the start of the movement, and (3) an early increase of negativity contralateral to a relevant stimulus (200-300 ms after stimulus onset) that was maximal at temporo-parietal sites but was also visible at central sites. Although related to stimulus side, this asymmetry was modulated by response requirements: it was largely abolished with simple responses, smaller with nogo than with Go stimuli and occurred twice when a sequence of simple and choice responses was required. Therefore, the early temporo-parietal asymmetry most probably reflects an interface between sensory and movement-related processes.     

Saccadic gain modification: visual error drives motor adaptation

The brain maintains the accuracy of saccadic eye movements by adjusting saccadic amplitude relative to the target distance (i.e., saccade gain) on the basis of the performance of recent saccades. If an experimenter surreptitiously moves the target backward during each saccade, thereby causing the eyes to land beyond their targets, saccades undergo a gradual gain reduction. The error signal driving this conventional saccadic gain adaptation could be either visual (the postsaccadic distance of the target from the fovea) or motoric (the direction and size of the corrective saccade that brings the eye onto the back-stepped target). Similarly, the adaptation itself might be a motor adjustment (change in the size of saccade for a given perceived target distance) or a visual remapping (change in the perceived target distance). We studied these possibilities in experiments both with rhesus macaques and with humans. To test whether the error signal is motoric, we used a paradigm devised by Heiner Deubel. The Deubel paradigm differed from the conventional adaptation paradigm in that the backward step that occurred during the saccade was brief, and the target then returned to its original displaced location. This ploy replaced most of the usual backward corrective saccades with forward ones. Nevertheless, saccadic gain gradually decreased over hundreds of trials. Therefore, we conclude that the direction of saccadic gain adaptation is not determined by the direction of corrective saccades. To test whether gain adaptation is a manifestation of a static visual remapping, we decreased the gain of 10 degrees horizontal saccades by conventional adaptation and then tested the gain to targets appearing at retinal locations unused during adaptation. To make the target appear in such "virgin territory," we had it jump first vertically and then 10 degrees horizontally; both jumps were completed and the target spot extinguished before saccades were made sequentially to the remembered target locations. Conventional adaptation decreased the gain of the second, horizontal saccade even though the target was in a nonadapted retinal location. In contrast, the horizontal component of oblique saccades made directly to the same virgin location showed much less gain decrease, suggesting that the adaptation is specific to saccade direction rather than to target location. Thus visual remapping cannot account for the entire reduction of saccadic gain. We conclude that saccadic gain adaptation involves an error signal that is primarily visual, not motor, but that the adaptation itself is primarily motor, not visual.     

Luminance and spatial attention effects on early visual processing

Event-related potentials (ERPs) were recorded from healthy subjects in response to unilaterally flashed high and low luminance bar stimuli presented randomly to left and right field locations. Their task was to covertly and selectively attend to either the left or right stimulus locations (separate blocks) in order to detect infrequent shorter target bars of either luminance. Independent of attention, higher stimulus luminance resulted in higher ERP amplitudes for the posterior N95 (80-110 ms), occipital P1 (110-140 ms), and parietal N1 (130-180 ms). Brighter stimuli also resulted in shorter peak latency for the occipital N1 component (135-220 ms); this effect was not observed for the N1 components over parietal, central or frontal regions. Significant attention-related amplitude modulations were obtained for the occipital P1, occipital, parietal and central N1, the occipital and parietal P2, and the parietal N2 components; these components were larger to stimuli at the attended location. In contrast to the relatively short latencies of both spatial attention and luminance effects, the first interaction between luminance and spatial attention effects was observed for the P3 component to the target stimuli (350-750 ms). This suggests that interactions of spatial attention and stimulus luminance previously reported for reaction time measures may not reflect the earliest stages of sensory/perceptual processing. Differences in the way in which luminance and attention affected the occipital P1, occipital N1 and parietal N1 components suggest dissociations among these ERPs in the mechanisms of visual and attentional processing they reflect.(ABSTRACT TRUNCATED AT 250 WORDS)     

Analysis of saccadic short-term plasticity in three dimensions

The capacity for short-term adaptation is a well-established property of the horizontal (H) and vertical (V) components of saccades. It allows these directional components, which clearly serve the goal of foveation, to maintain their precision even under changing circumstances. Torsional (T) saccade components, on the other hand, which deal with the orientation of the target on the fovea, have hardly been investigated in adaptation experiments. They appear to be severely restricted by Listing's law during fixations and saccades. The main purpose of Listing's law is far from obvious but could be visual or oculomotor. Better knowledge of the adaptive capacity of the saccadic system in the torsional direction could throw new light on the functional significance of this interesting neural strategy. To study short-term plasticity in the torsional components of saccades, binocular 3D-eye positions were measured, using magnetic search coils. Five normal human subjects were instructed to make uni-directional refixation saccades, while they viewed a large visual scene. To induce a change in the torsional component, the complete stimulus was rapidly rotated during these saccades. We thoroughly investigated the torsional responses of the saccadic system, to see if any short-term adaptive response in torsional direction was induced, in which case the notion of a visual purpose for Listing's law would be strengthened. In none of our experiments, however, did we find any clear adaptive response in torsional direction. To further investigate the reliability of this result and to ascertain that our experimental conditions allowed classical gain adaptation, we also did experiments designed to achieve a combination of torsional adaptation and classic gain shortening in one of the directional components. While gain adaptation was very obvious, none of the experiments provided evidence for a short-term effect in torsion. We conclude that our experiments do not support a purely visual basis for Listing's law.     

4 T-fMRI study of nonspatial shifting of selective attention: cerebellar and parietal contributions

Regional blood oxygenation in the cerebellum and posterior cerebral cortices was monitored with functional magnetic resonance imaging (fMRI) at four Tesla while 16 normal subjects performed three tasks with identical visual stimulation: fixation; attention focused upon either stimulus shape or color and sustained during blocks of trials (sustained attention); and rapid, serial shifts in attention between stimulus shape or color within blocks of trials (shifting attention). The stimuli were displayed centrally for 100 ms followed by a central fixation mark for 900 ms. Each stimulus was either a circle or a square displayed in either red or green. Attention shifting required switching between color and shape information after each target detection and occurred on average once every three seconds. Subjects pressed a response key upon detecting the target; reaction time and response accuracy were recorded. Two protocols for T2*-weighted echo-planar imaging were optimized, one with a surface coil for the cerebellum alone and the other with a volume coil for imaging both cerebellum and posterior brain structures (parietal, occipital, and part of temporal cortices). Because fMRI of the cerebellum is particularly susceptible to cardiac and respiratory fluctuations, novel techniques were applied to isolate brain activation signals from physiological noise. Functional activation maps were generated for contrasts of 1) sustained attention to color minus fixation; 2) sustained attention to shape minus fixation; and 3) shifting attention minus sustained attention (to color and shape; i.e., summed across blocks of trials). Consistent with the ease of these tasks, subjects performed with >80% accuracy during both sustained attention and shifting attention. Analysis of variance did not show significant differences in false alarms or true hits across either attentional condition. A subgroup of subjects whose performance data were recorded during ten minutes of continuous practice did not show significant changes over time. Both contrasts between the conditions of sustained attention to color or to shape as compared with the fixation condition showed significant bilateral activation in occipital and inferior temporal regions (Brodmann areas 18, 19, and 37). The anterior medial cerebellum was also significantly activated ipsilateral to the finger used for responding. The principal comparison of interest, the contrast between the condition of shifting attention and the condition of sustained attention produced significant and reproducible activation: lateral cerebellar hemisphere (ansiform lobule: Crus I Anterior and Crus I Posterior; left Crus I Posterior); cerebellar folium; posterior superior parietal lobule (R and L); and cuneus and precuneus (R and L).     

Postsaccadic enhancement of initiation of smooth pursuit eye movements in monkeys

Step-ramp target motion evokes a characteristic sequence of presaccadic smooth eye movement in the direction of the target ramp, catch-up targets to bring eye position close to the position of the moving target, and postsaccadic eye velocities that nearly match target velocity. I have analyzed this sequence of eye movements in monkeys to reveal a strong postsaccadic enhancement of pursuit eye velocity and to document the conditions that lead to that enhancement. Smooth eye velocity was measured in the last 10 ms before and the first 10 ms after the first saccade evoked by step-ramp target motion. Plots of eye velocity as a function of time after the onset of the target ramp revealed that eye velocity at a given time was much higher if measured after versus before the saccade. Postsaccadic enhancement of pursuit was recorded consistently when the target stepped 3 degrees eccentric on the horizontal axis and moved upward, downward, or away from the position of fixation. To determine whether postsaccadic enhancement of pursuit was invoked by smear of the visual scene during a saccade, I recorded the effect of simulated saccades on the presaccadic eye velocity for step-ramp target motion. The 3 degrees simulated saccade, which consisted of motion of a textured background at 150 degrees/s for 20 ms, failed to cause any enhancement of presaccadic eye velocity. By using a strategically selected set of oblique target steps with horizontal ramp target motion, I found clear enhancement for saccades in all directions, even those that were orthogonal to target motion. When the size of the target step was varied by up to 15 degrees along the horizontal meridian, postsaccadic eye velocity did not depend strongly either on the initial target position or on whether the target moved toward or away from the position of fixation. In contrast, earlier studies and data in this paper show that presaccadic eye velocity is much stronger when the target is close to the center of the visual field and when the target moves toward versus away from the position of fixation. I suggest that postsaccadic enhancement of pursuit reflects activation, by saccades, of a switch that regulates the strength of transmission through the visual-motor pathways for pursuit. Targets can cause strong visual motion signals but still evoke low presaccadic eye velocities if they are ineffective at activating the pursuit system.     

Expression and epitopic conservation of calponin in different smooth muscles and during development

The synaptic organization of the saccade-related neuronal circuit between the superior colliculus (SC) and the brainstem saccade generator was examined in an awake monkey using a saccadic, midflight electrical-stimulation method. When microstimulation (50-100 microA, single pulse) was applied to the SC during a saccade, a small, conjugate contraversive eye movement was evoked with latencies much shorter than those obtained by conventional stimulation. Our results may be explained by the tonic inhibition of premotor burst neurons (BNs) by omnipause neurons that ceases during saccades to allow BNs to burst. Thus, during saccades, signals originating from the SC can be transmitted to motoneurons and seen in the saccade trajectory. Based on this hypothesis, we estimated the number of synapses intervening between the SC and motoneurons by applying midflight stimulation to the SC, the BN area, and the abducens nucleus. Eye position signals were electronically differentiated to produce eye velocity to aid in detecting small changes. The mean latencies of the stimulus-evoked eye movements were: 7.9 +/- 1.0 ms (SD; ipsilateral eye) and 7.8 +/- 0.9 ms (SD; contralateral eye) for SC stimulation; 4.8 +/- 0.5 ms (SD; ipsilateral eye) and 5.1 +/- 0.7 ms (SD; contralateral eye) for BN stimulation; and 3.6 +/- 0.4 ms (SD; ipsilateral eye) and 5.2 +/- 0.8 ms (SD; contralateral eye) for abducens nucleus stimulation. The time difference between SC- and BN-evoked eye movements (about 3 ms) was consistent with a disynaptic connection from the SC to the premotor BNs.