Contribution of the rostral fastigial nucleus to the control of orienting gaze shifts in the head-unrestrained cat

The implication of the caudal part of the fastigial nucleus (cFN) in the control of saccadic shifts of the visual axis is now well established. In contrast a possible involvement of the rostral part of the fastigial nuceus (rFN) remains unknown. In the current study we investigated in the head-unrestrained cat the contribution of the rFN to the control of visually triggered saccadic gaze shifts by measuring the deficits after unilateral muscimol injection in the rFN. A typical gaze dysmetria was observed: gaze saccades directed toward the inactivated side were hypermetric, whereas those with an opposite direction were hypometric. For both movement directions, gaze dysmetria was proportional to target retinal eccentricity and could be described as a modified gain in the translation of visual signals into eye and head motor commands. Correction saccades were triggered when the target remained visible and reduced the gaze fixation error to 2.7 +/- 1.3 degrees (mean +/- SD) on average. The hypermetria of ipsiversive gaze shifts resulted predominantly from a hypermetric response of the eyes, whereas the hypometria of contraversive gaze shifts resulted from hypometric responses of both eye and head. However, even in this latter case, the eye saccade was more affected than the motion of the head. As a consequence, for both directions of gaze shift the relative contributions of the eye and head to the overall gaze displacement were altered by muscimol injection. This was revealed by a decreased contribution of the head for ipsiversive gaze shifts and an increased head contribution for contraversive movements. These modifications were associated with slight changes in the delay between eye and head movement onsets. Inactivation of the rFN also affected the initiation of eye and head movements. Indeed, the latency of ipsiversive gaze and head movements decreased to 88 and 92% of normal, respectively, whereas the latency of contraversive ones increased to 149 and 145%. The deficits induced by rFN inactivation were then compared with those obtained after muscimol injection in the cFN of the same animals. Several deficits differed according to the site of injection within the fastigial nucleus (tonic orbital eye rotation, hypermetria of ipsiversive gaze shifts and fixation offset, relationship between dysmetria and latency of contraversive gaze shifts, postural deficit). In conclusion, the present study demonstrates that the rFN is involved in the initiation and the control of combined eye-head gaze shifts. In addition our findings support a functional distinction between the rFN and cFN for the control of orienting gaze shifts. This distinction is discussed with respect to the segregated fastigiofugal projections arising from the rFN and cFN.     

Compensation for gaze perturbation during inactivation of the caudal fastigial nucleus in the head-unrestrained cat

Muscimol injection in the caudal part of the fastigial nucleus (cFN) leads, in the head-unrestrained cat, to a characteristic dysmetria of saccadic gaze shifts toward visual targets. The goal of the current study was to test whether this pharmacological cFN inactivation impaired the ability to compensate for unexpected perturbations in gaze position during the latency period of the saccadic response. Such perturbations consisted of moving gaze away from the target by a transient electrical microstimulation in the deep layers of the superior colliculus simultaneously with extinction of the visual target. After injection of muscimol in the cFN, targets located in the contralesional hemifield elicited gaze shifts that fell short of the target in both "perturbed" and "unperturbed" trials. The amplitude of the compensatory contraversive gaze shifts in perturbed trials coincided with the predicted amplitude of unperturbed responses starting from the same position. Targets located in the opposite hemifield elicited hypermetric gaze shifts in both trial types, and the error of compensatory responses was not statistically different from that of unperturbed gaze shifts. These results indicate that inactivation of the cFN does not interfere with the ability of the head-unrestrained cat to compensate for ipsiversive or contraversive perturbations in gaze position. Thus the gaze-related feedback signals that are used to compute a reference signal of desired gaze displacement are not impaired by cFN inactivation.     

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.     

Human oculomotor system accounts for 3-D eye orientation in the visual-motor transformation for saccades

A recent theoretical investigation has demonstrated that three-dimensional (3-D) eye position dependencies in the geometry of retinal stimulation must be accounted for neurally (i.e., in a visuomotor reference frame transformation) if saccades are to be both accurate and obey Listing's law from all initial eye positions. Our goal was to determine whether the human saccade generator correctly implements this eye-to-head reference frame transformation (RFT), or if it approximates this function with a visuomotor look-up table (LT). Six head-fixed subjects participated in three experiments in complete darkness. We recorded 60 degrees horizontal saccades between five parallel pairs of lights, over a vertical range of +/-40 degrees (experiment 1), and 30 degrees radial saccades from a central target, with the head upright or tilted 45 degrees clockwise/counterclockwise to induce torsional ocular counterroll, under both binocular and monocular viewing conditions (experiments 2 and 3). 3-D eye orientation and oculocentric target direction (i.e., retinal error) were computed from search coil signals in the right eye. Experiment 1: as predicted, retinal error was a nontrivial function of both target displacement in space and 3-D eye orientation (e.g., horizontally displaced targets could induce horizontal or oblique retinal errors, depending on eye position). These data were input to a 3-D visuomotor LT model, which implemented Listing's law, but predicted position-dependent errors in final gaze direction of up to 19.8 degrees. Actual saccades obeyed Listing's law but did not show the predicted pattern of inaccuracies in final gaze direction, i.e., the slope of actual error, as a function of predicted error, was only -0. 01 +/- 0.14 (compared with 0 for RFT model and 1.0 for LT model), suggesting near-perfect compensation for eye position. Experiments 2 and 3: actual directional errors from initial torsional eye positions were only a fraction of those predicted by the LT model (e. g., 32% for clockwise and 33% for counterclockwise counterroll during binocular viewing). Furthermore, any residual errors were immediately reduced when visual feedback was provided during saccades. Thus, other than sporadic miscalibrations for torsion, saccades were accurate from all 3-D eye positions. We conclude that 1) the hypothesis of a visuomotor look-up table for saccades fails to account even for saccades made directly toward visual targets, but rather, 2) the oculomotor system takes 3-D eye orientation into account in a visuomotor reference frame transformation. This transformation is probably implemented physiologically between retinotopically organized saccade centers (in cortex and superior colliculus) and the brain stem burst generator.     

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)     

Frames of reference and control parameters in visuomanual pointing.

Three hypotheses concerning the control variables in visuomanual pointing were tested. Participants pointed to a visual target presented briefly in total darkness on the horizontal plane. The starting position of the hand alternated randomly among 4 points arranged as a diamond. Results show that during the experiment, movement drifted from hypometric to hypermetric. Final positions depended on the starting position. Their average pattern reproduced the diamond of the starting points, either in same orientation (hypometric trials), or with a double inversion (hypermetric trials). The distribution of variable errors was elliptical, with the major axis aligned with the direction of the movement. Statistical analysis and Monte Carlo simulations showed that the results are incompatible with the final point control hypothesis (A. Polit & E. Bizzi, 1979). Better, but not fully satisfactory, agreement was found with the view that pointing involves comparing initial and desired postures (J. F. Soechting & M. Flanders, 1989a). The hypothesis that accounted best for the results is that final hand position is coded as a vector represented in an extrinsic frame of reference centered on the hand. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Response properties of saccade-related burst neurons in the central mesencephalic reticular formation

We studied the activity of saccade-related burst neurons in the central mesencephalic reticular formation (cMRF) in awake behaving monkeys. In experiment 1, we examined the activity of single neurons while monkeys performed an average of 225 delayed saccade trials that evoked gaze shifts having horizontal and vertical amplitudes between 2 and 20 degrees . All neurons studied generated high-frequency bursts of activity during some of these saccades. For each neuron, the duration and frequency of these bursts of activity reached maximal values when the monkey made movements within a restricted range of horizontal and vertical amplitudes. The onset of the movement followed the onset of the burst by the longest intervals for movements within a restricted range of horizontal and vertical amplitudes. The range of movements for which this interval was longest varied from neuron to neuron. Across the population, these ranges included nearly all contraversive saccades with horizontal and vertical amplitudes between 2 and 20 degrees. In experiment 2, we used the following task to examine the low-frequency prelude of activity that cMRF neurons generate before bursting: the monkey was required to fixate a light-emitting diode (LED) while two eccentric visual stimuli were presented. After a delay, the color of the fixation LED was changed, identifying one of the two eccentric stimuli as the saccadic target. After a final unpredictable delay, the fixation LED was extinguished and the monkey was reinforced for redirecting gaze to the identified saccadic target. Some cMRF neurons fired at a low frequency during the interval after the fixation LED changed color but before it was extinguished. For many neurons, the firing rate during this interval was related to the metrics of the movement the monkey made at the end of the trial and, to a lesser degree, to the location of the eccentric stimulus to which a movement was not directed.     

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.     

Optimizing gaze control in three dimensions

Horizontal and vertical movements of the human eye bring new objects to the center of the visual field, but torsional movements rotate the visual world about its center. Ocular torsion stays near zero during head-fixed gaze shifts, and eye movements to visual targets are thought to be driven by purely horizontal and vertical commands. Here, analysis of eye-head gaze shifts revealed that gaze commands were three-dimensional, with a separate neural control system for torsion. Active torsion optimized gaze control as no two-dimensional system could have, stabilizing the retinal image as quickly as possible when it would otherwise have spun around the fixation point.     

Directional organization of eye movement and visual signals in the floccular lobe of the monkey cerebellum

The floccular lobe of the monkey is critical for the generation of visually-guided smooth eye movements. The present experiments reveal physiological correlates of the directional organization in the primate floccular lobe by examining the selectivity for direction of eye motion and visual stimulation in the firing of individual Purkinje cells (PCs) and mossy fibers. During tracking of sinusoidal target motion along different axes in the frontoparallel plane, PCs fell into two classes based on the axis that caused the largest modulation of simple-spike firing rate. For "horizontal" PCs, the response was maximal during horizontal eye movements, with increases in firing rate during pursuit toward the side of recording (ipsiversive). For "vertical" PCs, the response was maximal during eye movement along an axis just off pure vertical, with increases in firing rate during pursuit directed downward and slightly contraversive. During pursuit of target motion at constant velocity, PCs again fell into horizontal and vertical classes that matched the results from sinusoidal tracking. In addition, the directional tuning of the sustained "eye velocity" and transient "visual" components of the neural responses obtained during constant velocity tracking were very similar. PCs displayed very broad tuning approximating a cosine tuning curve; the mean half-maximum bandwidth of their tuning curves was 170-180 degrees. Other cerebellar elements, related purely to eye movement and presumed to be mossy fibers, exhibited tuning approximately 40 degrees narrower than PCs and had best directions that clustered around the four cardinal directions. Our data indicate that the motion signals encoded by PCs in the monkey floccular lobe are segregated into channels that are consistent with a coordinate system defined by the vestibular apparatus and eye muscles. The differences between the tuning properties exhibited by PCs compared with mossy fibers indicate that a spatial transformation occurs within the floccular lobe.     

Properties of memory-guided saccades toward targets flashed during smooth pursuit in human subjects

PURPOSE: This study in human subjects investigated whether or not the saccade system can monitor smooth changes of the eye position in total darkness. METHODS: The authors studied the properties of memory-guided saccades toward targets flashed during pursuit eye movements (target velocities of 15 degrees/s, 30 degrees/s, and 45 degrees/s) in four normal human subjects. Subjects were instructed to execute memory-guided saccades toward the position of the flashed target in total darkness when the pursuit target was extinguished. RESULTS: The vector of the saccade was more highly correlated with the vector of "spatial error" (the vector from the position of the eye at the time of the saccade to the position of the flashed target in space) than with the vector of "retinal error" (the vector from the position of the eye at the time of the presentation of the flashed target to the position of the flashed target). The amplitude and direction errors of memory-guided saccades were correlated with the amplitude of the retinal error but not with amplitude of eye deviation after the presentation of the flashed target. Pursuit velocity did not affect the error of the saccade. CONCLUSIONS: These findings suggest that the saccade system can monitor smooth changes of the eye position in total darkness, regardless of the velocity of pursuit, and that the accuracy of memory-guided saccades is dependent only on the amplitude of the retinal error.     

Eye-head coordination toward auditory and visual targets in humans

Eye-head coordination during gaze orientation toward auditory targets in total darkness has been examined in human subjects. The findings have been compared, for the same subjects, with those obtained by using visual targets. The use of auditory targets when investigating eye-head coordination has some advantages with respect to the more common use of visual targets: (i) more eccentric target positions can be presented to the subject; (ii) visual feedback is excluded during the execution of gaze displacement; (iii) complex patterns of saccadic responses can be elicited. This last aspect is particularly interesting for examining the coupling between the eyes and the head displacements. The experimental findings indicate that during gaze orientation toward a visual or an auditory target the central nervous system adopts the same strategy of using both the saccadic mechanism and the head motor plant. In spite of a common strategy, qualitative and quantitative parameters of the resulting eye-head coordination are slightly different, depending on the nature of the target. The findings relating to patterns of eye-head coordination seem to indicate a dissociation between the eyes and the head, which receive different motor commands independently generated from the gaze error signal. The experimental findings reported in this paper have been summarized in a model of the gaze control system that makes use of a gaze feedback hypothesis through the central reconstruction of the eye and head positions.     

Eye-head coordination in labyrinthine-defective humans

Eye-head coordination during saccadic gaze shifts normally relies on vestibular information. A vestibulo-saccadic reflex (VSR) is thought to reduce the eye-in-head saccade to account for current head movement, and the vestibulo-ocular reflex (VOR) stabilizes postsaccadic gaze while the head movement is still going on. Acute bilateral loss of vestibular function is known to cause overshoot of gaze saccades and postsaccadic instability. We asked how patients suffering from chronic vestibular loss adapt to this situation. Eye and head movements were recorded from six patients and six normal control subjects. Subjects tracked a random sequence of horizontal target steps, with their heads (1) fixed in primary position, (2) free to move, or (3) preadjusted to different head-to-target offsets (to provoke head movements of different amplitudes). Patients made later and smaller head movements than normals and accepted correspondingly larger eye eccentricities. Targeting accuracy, in terms of the mean of the signed gaze error, was better in patients than in normals. However, unlike in normals, the errors of patients exhibited a large scatter and included many overshoots. These overshoots cannot be attributed to the loss of VSR because they also occurred when the head was not moving and were diminished when large head movements were provoked. Patients' postsaccadic stability was, on average, almost as good as that of normals, but the individual responses again showed a large scatter. Also, there were many cases of inappropriate postsaccadic slow eye movements, e.g., in the absence of concurrent head movements, and correction saccades, e.g., although gaze was already on target. Performance in patients was affected only marginally when large head movements were provoked. Except for the larger lag of the head upon the eye, the temporal coupling of eye and head movements in patients was similar to that in normals. Our findings show that patients with chronic vestibular loss regain the ability to make functionally appropriate gaze saccades. We assume, in line with previous work, three main compensatory mechanisms: a head movement efference copy, an active cervico-ocular reflex (COR), and a preprogrammed backsliding of the eyes. However, the large trial-to-trial variability of targeting accuracy and postsaccadic stability indicates that the saccadic gaze system of patients does not regain the high precision that is observed in normals and which appears to require a vestibular head-in-space signal. Moreover, this variability also permeates their gaze performance in the absence of head movements.     

Evidence for independent feedback control of horizontal and vertical saccades from Niemann-Pick type C disease

We measured the eye movements of three sisters with Niemann-Pick type C disease who had a selective defect of vertical saccades, which were slow and hypometric. Horizontal saccades, and horizontal and vertical pursuit and vestibular eye movements were similar to control subjects. The initial movement of oblique saccades was mainly horizontal and most of the vertical component occurred after the horizontal component ended; this resulted in strongly curved trajectories. After completion of the horizontal component of an oblique saccade, the eyes oscillated horizontally at 10-20 Hz until the vertical component ended. These findings are best explained by models that incorporate separate feedback loops for horizontal and vertical burst neurons, and in which the disease selectively affects vertical burst neurons.     

Tectal codification of eye movements in goldfish studied by electrical microstimulation. f

This work compares the tectal codification of eye movements in goldfish with those reported for other vertebrate groups. Focal electrical stimulation was applied in various tectal zones and the characteristics of evoked eye movements were examined as a function of (i) the position of the stimulation over the tectal surface, (ii) the initial position of the eyes and (iii) the parameters (pulse rate, current strength, duration) of the stimulus. In a large medial zone, stimulation within the intermediate and deep layers of the tectum evoked contraversive saccades of both eyes, whose direction and amplitude were roughly congruent with the retinotopic representation of the visual world within overlying layers. These saccades were minimally influenced by the initial position of the eye in the orbit. The topographical arrangement of evoked saccades and body movements suggests that this tectal zone triggers orienting responses in a similar way to those described in other vertebrates. Stimulations applied within the caudal tectum also evoked contraversive saccades, but in disagreement with the overlying retinotopic map--the vertical component was absent. Taken together with electrically evoked body movements reported in free-swimming fish, these saccades could reveal that this zone is involved in escape responses. When stimulations were applied within the anteromedial zone of the tectum, contraversive movements of both eyes appeared much more dependent on initial eye position. Saccades elicited from this area displayed characteristics of "goal-directed saccades" which were similar to those described in the cat. The generation of goal-directed movements from the anteromedial zone suggests that this portion of the goldfish optic tectum has a different intrinsic organization or is connected with the brainstem saccade generator in a different fashion than the medial zone. Finally, stimulation of the extreme anteromedial zone evoked convergent eye movements. These movements and those reported in free-swimming fish following electrical stimulation of this tectal area suggest that this zone could be involved in feeding responses. The relationships between the parameters of electrical stimulation and the characteristics of elicited saccades suggest that the stimulated location within the tectum determines a constant direction in the evoked saccade, whereas the amount and duration of tectal activity, as mimicked by changes in stimulus parameters, together with the tectal locus, determine the velocity and amplitude of the evoked saccade.     

Fixation conditions, the foveola and saccadic latency

Saccades are often elicited in the laboratory by the abrupt step-displacement of a single lit point which is initially the foveolar fixation point and then the eccentric refixation target. This was our Control condition. Four experiments modified the fixation arrangements to examine the effect of altered foveolar stimulation on saccadic latency and accuracy to targets within the central +/- 6 deg of the visual field. (1) No foveolar fixation point: The subject fixated the empty space midway between a pair of fixation guides, which later collapsed into a single refixation target. Latencies for small saccades were similar to the Control values. (2) No foveolar fixation point and no real refixation target: A pair of fixation guides underwent a yoked displacement, and it was easy to fixate and track the invisible midpoint. The smallest saccades were hypermetric, and the typical pattern of latency variation with retinal eccentricity was exaggerated in scale. (3) Spatial effects of a persistent non-target: The precise position of a non-target was important, latency increases being in the ipsilateral hemifield when the non-target was intrafoveolar and unilateral, bilateral when intrafoveolar and on the midline, and local when the non-target was extrafoveolar. (4) Temporal effects of a foveolar fixation point: Blanking an otherwise persistent fixation point for as little as 1 msec at the time of target presentation reduced the expected latency increase. We conclude that the position and timing of foveolar illumination can be critical for saccades of all sizes.     

Perception of everyday visual environments during saccadic eye movements

Subjects were required to execute saccadic eye movements in the horizontal plane which passed through primary gaze. During the saccades, visual images were projected onto a screen which subtended 40 degrees horizontaloy and 26 degrees vertically and was centered on primary gaze. Content, contrast, and intensity of the stimulus patterns and level of illumination of the laboratory background were manipulated to maximise pattern recognition. Little or no detail of the projected images could be discerned under any conditions. Only horizontal laminations were perceived as blurs of appropriate colour. It is concluded that there is no useful perception of the everyday environment during saccades.     

The elastic cartilage in the normal rat epiglottis. I. Fine structure

Unilateral electrolytic lesions of the locus coeruleus in rats result in spontaneous ipsiversive rotation, which is then replaced by contraversive rotation. One week after lesioning, when spontaneous turning ceases, apomorphine and d-amphetamine elicit contraversive circling behaviour, which was not affected by noradrenergic receptor blockade but was abolished by dopamine receptor blockade. The drug-induced contraversive circling response was also reproduced by piribedil but not clonidine. Combined unilateral electrolytic locus coeruleus and substantia nigra lesions on the same side resulted in apomorphine- and d-amphetamine-induced ipsilateral rotational behaviour which was indistinguishable from that seen with substantia nigra lesions alone. In rats with unilateral locus coeruleus lesions, the dose of intrastriatally injected apomorphine required to produce circling was less on the lesioned than the non-lesioned side. Direct injection of noradrenaline into one substantia nigra caused contraversive circling. Direct injection of phenoxybenzamine into one substantia nigra followed by apomorphine caused ipsiversive circling. The results suggest that the circling behaviour seen after unilateral locus coeruleus lesions depends on an asymmetry of striatal dopamine receptor activity and are consistent with a proposed coeruleus-nigral noradrenergic pathway, which enhances impulse flow in the dopaminergic nigrostriatal system.     

Morphological studies on Mn-SOD, NOS and calcium binding proteins in the rat hippocampus

Head movement propensity-the pattern of head saccades dependent on methods of target presentation-varies among individuals. The present group of 9 young adults was previously ranked in a visual saccadic task according to this propensity. The present report examines how and why this propensity changes if the saccades are made to auditory targets. 1) Spatially identical, interleaved, auditorily and visually elicited horizontal saccadic gaze shifts (jumps) differed in amplitude and in starting and/or ending position. The jumps were executed in two head movement modes: first, the non-aligned mode was a standard reaction-time single gaze step between two points. Second, the head-aligned mode required alignment of the head with the fixation (starting) point; thereafter both modes were identical. All results in the auditory task are expressed relative to the visual results. 2) In the non-aligned mode, head movement amplitudes were increased on average by 15% (for example, an 80 degrees jump elicited a 12 degrees larger head movement), and velocity decreased by 12%, reflecting the increased demands of the auditory task. More importantly, the differences between subjects was narrowed; that is, head movement propensity was homogenized in the auditory task. In the visual task, head-movers willingly move their heads off and across the midline, whereas non-movers are unwilling to leave the midline from eccentric starting points or to eccentric ending points. This is called the midline attraction effect and was previously linked to spatial reference frames. The homogenization in the auditory task was characterized by head-movers increasing, and non-movers decreasing, their midline attraction, suggesting altered spatial reference frames. 3) For heuristic purposes, the ideal head-mover is defined by a gain of 1.0 in the visual task, and by external earth-fixed reference frames. Similarly, the ideal non-mover has a gain of 0.0 and has a bias toward body (or some par of the body)-fixed reference frames. In the auditory task these gains (and reference frames) in head movers and non-movers are homogenized (close to 0.5), either by the participation of the head (movement of the ears in space) in sensory acquisition or by differences in central nervous processing of the two modalities, or both.     

Gaze-related activity of putative inhibitory burst neurons in the head-free cat

1. Previous studies in the cat have demonstrated that output neurons of the superior collicular as well as brain stem omnipause neurons have discharges that are best correlated, not with the trajectory of the eye in the head but, with the trajectory of the visual axis in space (gaze = eye-in-head + head-in-space) during rapid orienting coordinated eye and head movements. In this study, we describe the gaze-related activity of cat premotor "inhibitory burst neurons" (IBNs) identified on the basis of their position relative to the abducens nucleus. 2. The firing behavior of IBNs was studied during 1) saccades made with the head stationary, 2) active orienting combined eye-head gaze shifts, and 3) passive movements of the head on the body. IBN discharges were well correlated with the duration and amplitude of saccades made when the head was stationary. In both head-free paradigms, the behavior of cat IBNs differed from that of previously described primate "saccade bursters". The duration of their burst was better correlated with gaze than saccade duration, and the total number of spikes in a burst was well correlated with gaze amplitude and generally poorly correlated with saccade amplitude. The behavior of cat IBNs also differed from that of previously described primate "gaze bursters". The slope of the relationship between the total number of spikes and gaze amplitude observed during head-free gaze shifts was significantly lower than that observed during head-fixed saccades. 3. These studies suggest that cat IBNs do not fit into the categories of gaze-bursters or saccade-bursters that have been described in primate studies.(ABSTRACT TRUNCATED AT 250 WORDS)