Cortical control of saccades

Saccadic eye movements are controlled by a cortical network composed of several oculomotor areas that are now accurately localized. Clinical and experimental studies have enabled us to understand their specific roles better. These areas are: (1) the parietal eye field (PEF) located in the intraparietal sulcus involved in visuospatial integration and in reflexive saccade triggering; (2) the frontal eye field (FEF), located in the precentral gyrus, involved in the preparation and the triggering of purposive saccades; and (3) the supplementary eye field (SEF) on the medial wall of the frontal lobe, probably involved in the temporal control of sequences of visually guided saccades and in eye-hand coordination. A putative cingulate eye field (CEF), located in the anterior cingulate cortex, would be involved in motivational modulation of voluntary saccades. Besides these motor areas, the dorsolateral prefrontal cortex (dlPFC) in the midfrontal gyrus is involved in reflexive saccade inhibition and visual shortterm memory.     

Effects of repetitive transcranial magnetic stimulation over dorsolateral prefrontal and posterior parietal cortex on memory-guided saccades

We investigated the role of the dorsolateral prefrontal cortex (DLPFC) and the posterior parietal cortex (PPC) in a visuospatial delayed-response task in humans. Repetitive transcranial magnetic stimulation (20 Hz, 0.5 s) was used to interfere temporarily with cortical activity in the DLPFC and PPC during the delay period. Omnidirectional memory-guided saccades with a 3-s delay were used as a quantifiable motor response to a visuospatial cue. The question addressed was whether repetitive transcranial magnetic stimulation (rTMS) over the DLPFC or PPC during the sensory of memory phase affects accuracy of memory-guided saccades. Stimulation over the primary motor cortex served as control. Stimulation over the DLPFC significantly impaired accuracy of memory-guided saccades in amplitude and direction. Stimulation over the PPC impaired accuracy of memory-guided saccades only when applied within the sensory phase (50 ms after cue offset), but not during the memory phase (500 ms after cue offset). These results provide further evidence for a parieto-frontal network controlling performance of visuospatial delayed-response tasks in humans. It can be concluded that within this network the DLPFC is mainly concerned with the mnemonic respresentation and the PPC with the sensory representation of spatially defined perceptual information. Received: 22 April 1996/Accepted: 16 June 1997     

Hypometric primary saccades of schizophrenics in a delayed-response task

In this study, the execution of delayed saccades in 15 DSM-III-R-schizophrenic patients and 15 normal subjects was investigated. While looking at a central fixation cross, a peripheral target was randomly presented at 10° eccentricity. Subjects were instructed to saccade to the target when the fixation cross was switched off after 500 ms. Two experiments were conducted: (a) a delayed-saccade task and, (b) a memoryguided saccade task, that is, the peripheral target was switched off together with the fixation cross. In the delayed-saccade task, amplitudes of regular saccades did not differ between schizophrenic patients and normals. In the memory-guided saccade task, schizophrenic subjects showed marked hypometric saccades. Incorrect delayed saccades (while the fixation cross was on) were also hypometric in schizophrenics, but not in normal controls. The final eye position, i.e., the position reached after the execution of correction saccades, however, did not differ between patients and controls. This means that schizophrenics show a deficit in the programming of primary saccades, if the fixation point and the peripheral target are (a) both visually presented or (b) both memorized. The results support the hypothesis that these saccades are the result of an averaging effect between the fixation point and the peripheral target. It is further hypothesized that these deficits might be explained by a lack of prefrontal inhibition of ocular fixation areas.     

Selective adaptation of internally triggered saccades made to visual targets

We examined whether internally triggered saccades made to a nonjumping target (I-saccades) could be adapted independently from externally triggered saccades induced by a jumping target (E-saccades). Five subjects made I-saccades between two fixed targets, one placed straight ahead and the other one positioned at an eccentricity of 17.5°. The peripheral target was displaced to an eccentricity of 8.75° during the saccadic movements toward this target. Amplitudes of the I-saccades made from the central to the peripheral target before and after adaptation were compared with each other. Saccadic amplitudes after adaptation were between 10% and 42% smaller than those before adaptation. E-saccades induced by a single target which jumped from straight ahead to the same peripheral target position as was used for the I-saccades were also measured before and after the adaptation of I-saccades. Amplitudes of E-saccades before and after adaptation were hardly different from each other except in one subject. The mean decreases in amplitude of the two types of saccades, averaged over all subjects, were 21% for I-saccades and 5% for E-saccades. These results show that I-saccades can be adapted to changed visual conditions while E-saccades remain unadapted. We conclude from this finding that I-saccades and E-saccades are generated by at least partially different neural mechanisms.     

Tests of two hypotheses to account for different-sized saccades during disjunctive gaze shifts

Rapid shifts of the point of visual fixation between objects that lie in different directions and at different depths require disjunctive eye movements. We tested whether the saccadic component of such movements is equal for both eyes (Hering’s law) or is unequal. We compared the saccadic pulses of abducting and adducting movements when horizontal gaze was shifted from a distant to a near target aligned on the visual axis of one eye (Müller paradigm) in ten normal subjects. We similarly compared horizontal saccades made between two distant targets lying in the same field of movement as during the Müller paradigm tests, and between targets lying symmetrically on either side of the midline, at near side of the midline, at near or far. We measured the ratio of the amplitude of the movements of each eye in corresponding directions due to the saccadic component, as well as corresponding ratios of peak velocity and peak acceleration. In response to a Müller test paradigm requiring about 17° of vergence, the change in position of the unaligned eye was typically twice the size of the corresponding movement of the aligned eye. The ratio of peak velocities for the unaligned/aligned eyes was about 1.5, which was greater than for saccades made between distant targets. The ratio of peak acceleration for unaligned/aligned eyes was about 1.0 during shifts from near to far and about 1.3 for shifts from far to near, these values being similar to corresponding ratios for saccades between distant targets. These measurements of peak acceleration indicate that the saccadic pulses sent to each eye during the Müller paradigm are more equal than would be deduced by comparing the changes in eye position. We retested five subjects to compare directly the peak acceleration of saccades made during the Müller paradigm with similar-sized ”conjugate” saccades made between targets at optical infinity. Saccades made during the Müller paradigm were significant slower (P<0.005) than similar-sized conjugate saccades; this indicated that the different-sized movements during Müller paradigm are not simply due differences in saccadic pulse size but are also influenced by the concurrent vergence movement. A model for saccade-vergence interactions, which incorporates equal saccadic pulses for each eye, and differing contributions from convergence and divergence, accounts for many of these findings. Received: 31 December 1998 / Accepted: 14 July 1999     

Impairment of extraretinal eye position signals after central thalamic lesions in humans

Accuracy of four different types of memory-guided saccades was studied in two patients with a small central thalamic lesion, probably involving the region of the internal medullary lamina (IML), and in a control group. In the first paradigm, the eyes and head remained immobile between the time of the presentation of the visual target to be remembered and the memory-guided saccade. In the other three paradigms, the eyes were displaced during the same period (before the memory-guided saccade) by either visually-guided saccades, a smooth pursuit eye movement or a body movement (with vestibulo-ocular reflex suppression). Therefore, in these three paradigms, the initial eye displacement required the use of extraretinal eye position to produce accurate memory-guided saccades. Compared with the control group, the two patients had normal accuracy in the first memory-guided saccade paradigm, in which there was no initial eye displacement, but markedly impaired saccade accuracy in the other three paradigms. These results suggest that the cortical areas triggering saccades did not receive correct extraretinal eye position signals. They are consistent with an impairment of the efference copy, which could be distributed to the cortical ocular motor areas by the IML.     

Effects of spatial attention on directional manual and ocular responses

 The aim of the present study was to investigate how spatial attention influences directional manual and saccadic reaction times. Two experiments were carried out. In experiment 1 subjects were instructed to perform pointing responses toward targets that were located either in the same or the opposite hemifield with respect to the hemifield in which an imperative stimulus was presented. In experiment 2, they were instructed to make saccadic or pointing responses. The direction of the responses was indicated by the shape of the imperative stimulus. Reaction time (RT), movement time, and, in experiment 2, saccadic trajectory were measured. The imperative stimulus location was either cued (endogenous attention) or uncued. In the latter case the imperative stimulus presentation attracted attention (exogenous attention). The main results of the experiments were the following: First, exogenous attention markedly decreased the RTs when the required movement was directed toward the imperative stimulus location. This directional effect was much stronger for pointing than for ocular responses. Second, endogenously allocated attention did not influence differentially RTs of pointing responses directed toward or away the attended hemifield. In contrast, endogenous attention markedly favored the saccadic responses when made away from the cued hemifield. Third, regardless of cueing, the direction of movement affected both pointing and saccadic reaction times. Saccadic reaction times were faster when the required movement was directed upward, while manual reaction times were faster when the movement was directed downward. Fourth, lateralized spatial attention deviated the trajectory of the saccades contralateral to the attention location. This pattern of results supports the notion that spatial attention depends on the activation of the same sensorimotor circuits that program actions in space. Received: 11 June 1996 / Accepted: 26 October 1996     

The origin of ocular microtremor in man

 A novel technique for the study of human eye movements was used to investigate the frequency components of ocular drift and microtremor in both eyes simultaneously. The tangential components of horizontal eye accelerations were recorded in seven healthy subjects using light-weight accelerometers mounted on scleral contact lenses during smooth pursuit movements, vestibulo-ocular reflexes and eccentric gaze with and without fixation. Spectral peaks were observed at low (up to 25 Hz) and high (60–90 Hz) frequencies. A multivariate analysis based on partial coherence analysis was used to correct for head movement. After correction, the signals were found to be coherent between the eyes over both low- and high-frequency ranges, irrespective of task, convergence or fixation. It is concluded that the frequency content of ocular drift and microtremor reflects the patterning of low-level drives to the extra-ocular muscle motor units. Received: 24 November 1998 / Accepted: 18 February 1999     

Peak velocities of visually and nonvisually guided saccades in smooth-pursuit and saccadic tasks

 Smooth pursuit typically includes corrective catch-up saccades, but may also include such intrusive saccades away from the target as anticipatory or large overshooting saccades. We sought to differentiate catch-up from anticipatory and overshooting saccades by their peak velocities, to see whether the higher velocities of visually rather than nonvisually guided saccades in saccadic tasks may be found also in saccades in pursuit. In experiment 1, 12 subjects showed catch-up, anticipatory, and overshooting saccades to comprise 70.4% of all saccades in pursuit of periodic, 30°/s constant-velocity targets. Catch-up saccades were faster than the others. Saccadic tasks were run as well, on 19 subjects, including the 12 whose pursuit data were analyzed, with target-onset, target-remaining (saccade to the remaining target when the other three extinguish), and antisaccade tasks. For 17 of the 19 subjects, antisaccade velocities were lower than for either target-onset or target-remaining tasks. Velocities for the target-remaining task were near those for target onset, indicating that target presence, not its onset, defines visually guided saccades. Error and reaction-time data suggest greater cognitive difficulty for target remaining than for target onset, so that the cognitive difficulty of typical nonvisually guided saccade tasks is not sufficient to produce their lowered velocity. To produce reliably, in each subject, catch-up and anticipatory saccades with comparable amplitude distributions, nine new subjects were asked in experiment 2 to make intentional catch-up and anticipatory saccades in pursuit, and were presented with embedded target jumps to elicit catch-up saccades, all with periodic target trajectories of 15°/s and 30°/s. Velocities of intentional anticipatory saccades were lower than velocities of intentional catch-up saccades, while velocities of intentional and embedded catch-up saccades were similar. Target-onset and remembered-target saccadic tasks were run, showing the expected higher velocity for the target-onset task in each subject. Both experiments demonstrate higher peak velocities for catch-up saccades than for anticipatory saccades, suggesting that cortical structures preferentially involved in nonvisually guided saccades may initiate the anticipatory and overshooting saccades in pursuit. Received: 1 December 1995 / Accepted: 25 February 1997     

Combined deficits of saccades and visuo-spatial orientation after cortical lesions

Functionally, saccadic eye movements are closely linked to visuo-spatial orientation. Anatomically, the network of cortical areas controlling saccades also seems to be involved in spatial attention and orientation. Consequently, lesions should cause deficits in both categories. We investigated this in 34 patients with focal unilateral lesions of the posterior parietal cortex (PPC), the frontal eye fields (FEF), the supplementary motor area (SMA), or the dorsolateral prefrontal cortex (PFC). Saccadic eye movements were recorded using infrared reflection oculography. Visual hemineglect or other visuo-spatial disorders were investigated by a series of standardized paper-pencil tests. Further, the internal spatial coordinates (subjective visual vertical and subjective straight ahead) were assessed psychophysically. Depending on the site of the lesion, different patterns of deficits were identified: lesions of the PPC impaired reflexive exploration of visual space in terms of delayed and hypometric visually triggered saccades into the contralesional hemifield, related to the severity of visual hemineglect. Further, PPC lesions specifically affected basic functions of the perceptual analysis of space, such as the internal spatial coordinates and spatial constancy across saccades. The latter was tested by applying visual double-step stimuli, where saccade-related extraretinal information had to be taken into account for achieving spatial accuracy. Frontal lesions left these functions intact. FEF lesions, however, impaired systematic intentional exploration of space, thus causing an exploratory-motor type of visual hemineglect. Prefrontal (PFC) lesions impaired the working memory for saccade-related spatial information, and SMA lesions affected temporal properties such as the timing of saccadic sequences, but did not cause specific visuo-spatial deficits. In conclusion, patients with frontal or parietal cortical lesions often exhibit combined saccadic and visuo-spatial disorders, most of which are topically specific.     

Timing variability of repetitive saccadic eye movements

We assessed the suitability of using the Wing and Kristofferson model for timing repetitive motor responses to analyse timing variability during repetitive saccadic eye movements. The model decomposes total timing variability (TV) into a central timing component (CV) and a peripheral motor delay component (MV). Eight normal subjects made voluntary horizontal saccades, in darkness, in synchrony with a regular auditory metronome. After 20 saccades had been produced, the metronome was switched off and subjects continued responding at the same frequency until 31 further saccades had been made. Inter-saccade intervals (ISIs) from the unpaced phase were used to calculate TV, CV and MV. Three different target intervals, paced by auditory cues, were used – 496 ms, 752 ms and 1000 ms. In the paced phase, subjects’ ISIs closely matched the auditory cue intervals. In the unpaced phase, subjects were clearly able to respond at three different frequencies. As predicted by the Wing and Kristofferson model, the durations of successive ISIs tended to be negatively correlated. As expected, TV and CV increased with increasing ISI. Contrary to the expectation of the model that MV would remain constant, we found that it increased with increasing interval. Our results do not conclusively demonstrate the validity of applying the Wing and Kristofferson model to the analysis of timing variability during repetitive saccadic eye movements. However, comparison with previous studies shows that, at least in normal subjects, it is equally valid to apply the model to the analysis of repetitive saccadic eye movements as it is to apply it to the analysis of data from other effectors. Received: 5 December 1996 / Accepted: 3 November 1997     

Spontaneous object recognition and object location memory in rats: the effects of lesions in the cingulate cortices, the medial prefrontal cortex, the cingulum bundle and the fornix

 The first experiment assessed the effects of neurotoxic lesions in either the anterior cingulate cortex (ACc) or the retrosplenial cortex (RSc) on a test of object recognition. Neither lesion affected performance on this task, which takes advantage of the rat’s normal preference to spend more time investigating novel rather than familiar stimuli. In response to this negative result, a second experiment assessed the effects of much more extensive cingulate lesions (Cg) on both object recognition and object location memory. The latter task also used a preference measure, but in this case it concerned preference for a novel location. For comparison purposes this second study included groups of rats with lesions in closely allied regions: the fornix (Fx), the cingulum bundle (CB) and the medial prefrontal cortex (Pfc). Comparisons with sham-operated control rats showed that none of the four groups (Cg, Fx, CB, Pfc) was impaired on the object recognition task, adding further weight to the view that these structures are not necessary for assessing stimulus familiarity. The Fx and Cg groups were, however, impaired on the object location task, suggesting that these regions are necessary for remembering other attributes of a stimulus (spatial location). Received: 28 March 1996 / Accepted: 1 August 1996     

Influence of transcranial magnetic stimulation on the execution of memorised sequences of saccades in man

Memorised sequences of saccades are cortically controlled by the supplementary motor area (SMA), as shown in animal experiments and in humans with isolated SMA lesions. We applied transcranial magnetic stimulation (TMS) in eight healthy subjects executing memorised sequences of saccades. Sequences of three targets were presented. Then, upon a go-signal, the subjects had to execute the appropriate sequences. Ten to fifteen sequences were performed in each experiment, and the number of errors were counted. The number of errors increased significantly if TMS was given 80 ms before or 60 ms after the go-signal, with the stimulation coil overlying the SMA. There was no significant increase in errors if different stimulation intervals were chosen (160ms and 120ms before the go-signal; 100 ms, 140 ms or 240 ms after the go-signal), if the coil was positioned inappropriately (e.g. over the occipital cortex), or if the stimulator output was too low. We conclude that TMS can interfere specifically with the function of the SMA during a critical time interval close to the go-signal.     

Eye-position dependence of three-dimensional ocular rotation-axis orientation during head impulses in humans

 If horizontal saccades or smooth-pursuit eye movements are made with the line-of-sight at different elevations, the three-dimensional (3D) angular rotation axis of the globe tilts by half the vertical eye eccentricity. This phenomenon is named ”half-angle rule” and is a consequence of Listing’s law. It was recently found that the ocular rotation axis during the horizontal vestibulo-ocular reflex (VOR) on a turntable also tilts in the direction of the line-of-sight by about a quarter of the eye’s vertical eccentricity. This is surprising, since, in a ”perfect” VOR, the angular rotation axis of the eye should be independent from the position of the eye to fully compensate for the 3D angular head rotation. We asked whether this quarter-angle strategy is a general property of the VOR or whether the 3D kinematics of ocular movements evoked by vestibular stimulation would be less eye-position dependent at higher stimulus frequencies. Nine healthy subjects were exposed to horizontal head impulses (peak velocity ∼250°/s). The line-of-sight was systematically changed along the vertical meridian of a tangent screen. Three-dimensional eye and head movements were monitored with dual search coils. The 3D orientation of the angular eye-in-head rotation axis was determined by calculating the average angular velocity vectors of the initial 10° displacements. Then, the difference between the tilt angles of the ocular rotation axis during upward and downward viewing was determined and divided by the difference of vertical eccentricity (”tilt angle coefficient”). Control experiments included horizontal saccades, smooth-pursuit eye movements, and eye movements evoked by slow, passive head rotations at the same vertical eye eccentricities. On average, the ocular rotation axis during horizontal head-impulse testing at different elevations of the line-of-sight was closely aligned with the rotation axis of the head (tilt angle coefficient of pooled abducting and adducting eye movements: 0.11±0.17 SD). Values for slow head impulses, however, exceeded somewhat the quarter angle (0.33±0.12), while smooth-pursuit movements (0.50±0.09) and saccades (0.44±0.11) were closest to the half angle. These results demonstrate that the 3D orientation of the ocular rotation axis during rapid head thrusts is relatively independent of the direction of the line-of-sight and that ocular rotations elicited by head impulses are kinematically different from saccades, despite similar movement dynamics. Received: 17 July 1998 / Accepted: 17 May 1999     

Thalamic and temporal cortex input to medial prefrontal cortex in rhesus monkeys

 To determine the source of thalamic input to the medial aspect of the prefrontal cortex, we injected retrograde tracers (wheat germ agglutinin conjugated to horseradish peroxidase, nuclear yellow, and/or bisbenzimide) into seven medial prefrontal sites and anterograde tracers (tritiated amino acids) into six thalamic sites, in a total of nine rhesus monkeys. The results indicated that ventral precallosal and subcallosal areas 14 and 25, and the ventral, subcallosal part of area 32, all receive projections from the mediodorsal portion of the magnocellular division of the medial dorsal nucleus (MDmc). The dorsal, precallosal part of area 32 receives projections mainly from the dorsal portion of the parvocellular division of the medial dorsal nucleus (MDpc), which also provides some input to area 14. Polar area 10 receives input from both MDpc and the densocellular division of the medial dorsal nucleus (MDdc), as does supracallosal area 24. Area 24 receives additional input from the anterior medial nucleus and midline nuclei. All medial prefrontal cortical areas were also found to receive projections from a number of cortical regions within the temporal lobe, such as the temporal pole, superior temporal gyrus, and parahippocampal gyrus. Areas 24, 25, and 32 receive, in addition, input from the entorhinal cortex. Combining these results with prior anatomical and behavioral data, we conclude that medial temporal areas that are important for object recognition memory send information directly both to dorsal medial prefrontal areas 24 and 32 and to ventral medial prefrontal areas 14 and 25. Only the latter two areas have additional access to this information via projections from the mediodorsal part of MDmc. Received: 1 March 1996 / Accepted: 13 January 1997     

Reversible inactivation of macaque dorsomedial frontal cortex: effects on saccades and fixations

 Neural recording and electrical stimulation results suggest that the dorsomedial frontal cortex (DMFC) of macaque is involved in oculomotor behavior. We reversibly inactivated the DMFC using lidocaine and examined how saccadic eye movements and fixations were affected. The inactivation methods and monkeys were the same as those used in a previous study of the frontal eye field (FEF), another frontal oculomotor region. In the first stage of the present study, monkeys performed tasks that required the generation of single saccades and fixations. During 15 DMFC inactivations, we found only mild, infrequent deficits. This contrasts with our prior finding that FEF inactivation causes severe, reliable deficits in performance of these tasks. In the second stage of the study, we investigated whether DMFC inactivation affected behavior when a monkey was required to make more than one saccade and fixation. We used a double-step task: two targets were flashed in rapid succession and the monkey had to make two saccades to foveate the target locations. In each of five experiments, DMFC inactivation caused a moderate, significant deficit. Both ipsi- and contraversive saccades were disrupted. In two experiments, the first saccades were made to the wrong place and had increased latencies. In one experiment, first saccades were unaffected, but second saccades were made to the wrong place and had increased latencies. In the remaining two experiments, specific reasons for the deficit were not detected. Saline infusions into DMFC had no effect. Inactivation of FEF caused a larger double-step deficit than did inactivation of DMFC. The FEF inactivation impaired contraversive first or second saccades of the sequence. In conclusion, our results suggest that the DMFC makes an important contribution to generating sequential saccades and fixations but not single saccades and fixations. Compared with the FEF, the DMFC has a weaker, less directional, more task-dependent oculomotor influence. Received: 12 January 1998 / Accepted: 17 July 1998     

Deficits of gaze stability in multiple axes following unilateral vestibular lesions

 Abnormalities in the vestibulo-ocular reflex (VOR) after unilateral vestibular injury may cause symptomatic gaze instability. We compared five subjects who had unilateral vestibular lesions with normal control subjects. Gaze stability and VOR gain were measured in three axes using scleral magnetic search coils, in light and darkness, testing different planes of rotation (yaw and pitch), types of stimulus (sinusoids from 0.8 to 2.4 Hz, and transient accelerations) and methods of rotation (active and passive). Eye velocity during horizontal tests reached saturation during high-velocity/acceleration ipsilesional rotation. Rapid vertical head movements triggered anomalous torsional rotation of the eyes. Gaze instability was present even during active rotation in the light, resulting in oscillopsia. These abnormal VOR responses are a consequence of saturating nonlinearities, which limit the usefulness of frequency-domain analysis of rotational test data in describing these lesions. Received: 22 April 1996 / Accepted: 18 February 1997     

Local norepinephrine depletion and learning-related neuronal activity in cingulate cortex and anterior thalamus of rabbits

Summary Multi-unit neuronal activity was recorded in posterior cingulate cortex (area 29) and the anterior ventral (AV) thalamic nucleus during discriminative instrumental avoidance learning wherein a response (stepping in an activity wheel) to a 0.5-s tone (CS⁺) prevented a foot-shock 5 s after CS⁺ onset. Presentations of a different tone (CS^-) on 50% of the conditioning trials in an irregular sequence with the CS⁺ did not predict shock and thus required no response. Two groups of rabbits received intracranial micro-injections of 6-hydroxydopamine (6-OHDA) to locally deplete the NE in area 29 or the AV nucleus. Vehicle was injected in the non-depleted area in each group and a third group received vehicle injections in both areas. Dopamine neurons in subjects that received 6-OHDA were protected by pre-treatment with GBR-12909. Neuronal data were collected during two pre-training sessions in response to the tones only and when the tones and shock were presented unpaired. Thalamically depleted rabbits made more, and cortically depleted rabbits made fewer, avoidance responses than controls during the early stages of behavioral acquisition, and cortically depleted rabbits made fewer responses than controls and thalamically depleted rabbits during extinction testing administered after the completion of acquisition. One effect of NE depletion on neuronal activity was entirely local: elimination of neuronal sensitization effects (enhanced discharges elicited by tones during the unpaired tone-shock pre-training treatment relative to pre-training with tones only). Other neuronal effects of NE depletion were system-wide, i.e., they occurred whether the depletion was cortical or thalamic. These were: attenuation of area 29 tone-elicited neuronal discharges and enhancement of AV thalamic discharges before and during training; elimination in area 29 of neuronal discrimination between CS⁺ and CS^-, induced in controls by CS⁺-shock pairings in the first conditioning session; induction of this neuronal discrimination, not present in controls, in the AV nucleus during the first conditioning session; attenuation of discharge enhancements elicited in controls by unexpected stimuli (presentation of auditory stimuli different in quality and incidence from the CS⁺). Excepting the noted losses at the outset of training, the results did not support an involvement of NE in the production of cingulate cortical or AV thalamic excitatory and discriminative training-induced neuronal activity. The system-wide alterations due to NE depletion implicated NE in the processing of unexpected events and in the production of dynamic neuronal patterns relevant to mnemonic retrieval. Several of the depletion-related neuronal changes were similar to the effects of hippocampal formation (subicular) lesions, suggesting that NE-dependent functions in area 29 and the AV nucleus are governed by hippocampal efferents, which may control the release of NE in these areas.     

Enhanced activation of neurons in prelunate cortex before visually guided saccades of trained rhesus monkeys

Summary Single unit recording from trained rhesus monkeys demonstrate that the activity of the prelunate cortex is enhanced when a visual stimulus becomes a target of saccadic eye movement. As a rule, the enhancement is spatially selective: it does not occur if the animal makes an eye movement away from, rather than towards the stimulus. The results show that the prelunate cortex has access to an extraretinal signal which is activated in association with events preceding visually guided eye movements. Whether the signal reflects the initiation of eye movement or the animal's interest in the stimulus, which he usually selects to initiate an eye movement, remains uncertain.Supported by the Deutsche Forschungsgemeinschaft (DFG), Sonderforschungsbereich Hirnforschung und Sinnesphysiologie (SFB 70, Tp. B7)     

Amplitude criteria and anticipatory saccades during smooth pursuit eye movements in schizophrenia.

Increased frequency of anticipatory saccades during smooth pursuit eye movements is a potential marker of genetic risk for schizophrenia even in the absence of clinical symptomology. The operational definition of anticipatory saccades has often included an amplitude criterion; however, these amplitude criteria have often differed across studies. This study reports on the effect of varying amplitude criteria on the effect size in a comparison of 29 schizophrenic adults and 29 normal subjects during a 16.7 degrees/s constant velocity task. The inclusion of small amplitude anticipatory saccades, with amplitudes of 1-4 degrees, consistently increased effect size (largest effect size = 1.61). The inclusion of large anticipatory saccades, with amplitudes of 4 degrees or greater, had an inconsistent impact on effect size. The separation of anticipatory saccades into leading saccades (anticipatory saccades with amplitude 1-4 degrees) and large anticipatory saccades (amplitude > 4 degrees) deserves further exploration.