Nucleotide sequences and functional characterization of two tobacco UAG suppressor tRNA(Gln) isoacceptors and their genes

The hypothesis was tested that peak velocity of saccadic eye movements in visual motor tasks varies with variables related to energy regulation. The hypothesis is based on the cognitive-energetical performance model of Sanders. An experimental paradigm was developed in which saccadic peak velocity of task-relevant eye movements is measured while a choice reaction task is carried out. Confounding factors of saccadic amplitude and movement direction were controlled. The task was designed in such a way that in each trial subjects performed a target saccade towards an imperative stimulus and a return saccade after the manual response back to the centre of the screen. For both types of saccades the experimental variables were foreperiod duration (short versus long), knowledge of results (with versus without), postsaccadic demand (low versus high) and time on task (five 30-min intervals). In two experiments, there are main and interaction effects of the task variables on peak saccadic velocity. Return saccades are slower than target saccades, but not in the case of high postsaccadic demand. Knowledge of results increases peak saccadic velocity, but more so for return than for target saccades. Time on task leads to a decrease in peak saccadic velocity, which is much stronger for return than for target saccades; furthermore this effect is more pronounced after short than after long foreperiods. Peak saccadic velocity is changed within seconds. The results support the hypothesis. Peak saccadic velocity of task related eye movements reflects energy regulation during task performance. The paradigm will be developed as a diagnostic tool in workload measurement.     

Eye- and head movements in freely moving rabbits

1. Eye- and head movements were recorded in unrestrained, spontaneously behaving rabbits with a new technique, based upon phase detection of signals induced in implanted coils by a rotating magnetic field. 2. Movements of the eye in space were exclusively saccadic. In the intersaccadic intervals the eyes were stabilized in space, even during vigorous head movements. Most of this stability was maintained in darkness, except for the occurrence of slow drift. 3. Many saccades were initiated while the head was stationary. They were accompanied by a similar, but slower head rotation with approximately the same amplitude. The displacement of the eye in space was a pure step without appreciable under- or over-shoot. The deviation of the eye in the head was mostly transient. 4. Other saccades were started while the head was moving and were possibly fast phases of a vestibulo-ocular reflex. The time course of the eye movement in space was identical for all saccades, whether the head was moving prior to the saccade or not. Eye movements without any head movement were not observed. 5. Saccades were mostly large (average 20-6 +/- 12-4 degrees S.D.) and never smaller than 1 degree. The relations of maximal velocity and duration to amplitude were similar to those reported for man. 6. Visual pursuit of moving objects, when elicited, was only saccadic and never smooth. 7. It is concluded that the co-ordination and dynamics of the rabbit's head- and eye movements are similar to those of primates. In the absence of foveal specilization, the eye movements are restricted to a rather global redirection of the visual field, possibly in particular of the binocular area.     

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.     

A modification of eye-head coordination by CNS disease

When a subject, seated and facing ahead, was asked to look toward one side, the result was a combined movement of the eyes and head. Normal subjects began the eye movement just before the onset of head movement; 4 neurologic patients who showed abnormalities in eye movements (saccades that tended to be smaller in amplitude and lower in velocity than those of the control subjects) regularly began eye movement after the onset of head movement. Thus the initiation of the head rotation was not as much retarded in these patients as that of eye movement. Amplitudes of the movements were reduced in the patients, but this change too was less for the head than for the eyes. Because the amplitude and velocity of the head movement were less affected in the patient group, the relative contribution of the head to the total gaze shift was increased. It appears as if, when the oculomotor system is affected, the head can assume a leading role in the initiation and execution of gaze shifts.     

Memory-guided saccadic eye movements: effects of cerebellar disease

We compared the accuracy of oblique, memory-guided saccades if the eye is stationary or moves horizontally during the memory period. We studied 11 patients with cerebellar disease and 11 age-matched control subjects. Normal subjects showed similar accuracy of saccades for both conditions. In contrast, all patients showed greater errors if the eye moved horizontally during the memory period; however, errors of both vertical and horizontal components of memory-guided saccades were similar. Thus, inaccuracy of memory-guided saccades could not be simply attributed to failure to internally monitor change in horizontal gaze during the memory period. Instead, we propose that the greater saccadic errors which occurred when gaze changed during the memory period reflected a disruption of predictive mechanisms governing eye movements.     

Gain adaptation of eye and head movement components of simian gaze shifts

Gain adaptation of eye and head movement components of simian gaze shifts. J. Neurophysiol. 78: 2817-2821, 1997. To investigate the site of gaze adaptation in primates, we reduced the gain of large head-restrained gaze shifts made to 50 degrees target steps by jumping the target 40% backwards during a targeting saccade and then tested gain transfer to the eye- and head-movement components of head-unrestrained gaze shifts. After several hundred backstep trials, saccadic gain decreased by at least 10% in 8 of 13 experiments, which were then selected for further study. The minimum saccadic gain decrease in these eight experiments was 12.8% (mean = 18.4%). Head-unrestrained gaze shifts to ordinary 50 degrees target steps experienced a gain reduction of at least 9.3% (mean = 14.9%), a mean gain transfer of 81%. Both the eye and head components of the gaze shift also decreased. However, average head movement gain decreased much more (22.1%) than eye movement gain (9.2%). Also, peak head velocity generally decreased significantly (20%), but peak eye velocity either increased or remained constant (average increase of 5.6%). However, the adapted peak eye and head velocities were appropriate for the adapted, smaller gaze amplitudes. Similar dissociations in eye and head metrics occurred when head-unrestrained gaze shifts were adapted directly (n = 2). These results indicated that head-restrained saccadic gain adaptation did not produce adaptation of eye movement alone. Nor did it produce a proportional gain change in both eye and head movement. Rather, normal eye and head amplitude and velocity relations for a given gaze amplitude were preserved. Such a result could be explained most easily if head-restrained adaptation were realized before the eye and head commands had been individualized. Therefore, gaze adaptation is most likely to occur upstream of the creation of separate eye and head movement commands.     

Plasma secretin and pancreatic bicarbonate response to exogenous secretin in man

Saccadic and smooth eye movements are controlled by separate mechanisms within the nervous system. We describe a patient with familial ataxia, considered to be a form of olivopontocerebellar degeneration, who is incapable of generating reflex or voluntary saccades. She can, however, move her eyes smoothly to the normal limits of lateral gaze, even when her head is prevented from moving. Latency before onset of movement is prolonged, and the velocity of movement is abnormally slow. We postulate that the degenerative process may have affected selectively those cells of the ventral paramedian pontine tegmentum responsible for the generation of saccades; and the the prolonged latency from presentation of a visual stimulus to the onset of movement is related to an inability to generate burst discharges needed to overcome the viscoelastic properties of the orbital tissues.     

Saccades induced electrically from the dorsomedial frontal cortex: evidence for a head-centered representation

The amplitude and direction of saccadic eye movements evoked electrically from the dorsomedial frontal cortex (DMFC) of monkeys vary with starting eye position. This observation has been used to argue that the DMFC codes saccadic eye movements in head-centered coordinates. Whether the amplitude and direction of the evoked saccades are also affected by changes in head position has never been demonstrated. Such a result would argue against a head-centered representation, and instead would suggest a representation anchored to another body part. Tests were conducted on rhesus monkeys to determine whether changing the position of the head with respect to the trunk or changing the position of the head with respect to the gravitational axis alters saccadic parameters. The amplitude and direction of saccadic eye movements remained invariant to such manipulations. These findings confirm the claim that the DMFC encodes saccadic eye movements in head-centered coordinates.     

Torticollis due to disinhibition of the vestibulo-collic reflex in a patient with Steele-Richardson-Olszewski syndrome

A patient with the clinical picture of Steele-Richardson-Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low-amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained deviated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo-collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole-body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of approximately 30 ms.     

Eye tracking dysfunction in schizophrenia: Characterization of component eye movement abnormalities, diagnostic specificity, and the role of attention.

To characterize oculomotor components and diagnostic specificity of eye tracking abnormalities in schizophrenia, we examined a large consecutively admitted series of psychotic patients and matched controls. The most common abnormality in schizophrenic patients was low gain (slow) pursuit eye movements (47% of cases). Pursuit and saccadic eye movement abnormalities were no more severe in schizophrenic Ss than in those with affective psychoses, except that high rates of catch-up saccades were unique to schizophrenic Ss (17% of cases). These findings indicate that impaired pursuit eye movements are a major cause of eye tracking impairments in schizophrenia, that tracking dysfunctions commonly occur in affective psychoses, and that markedly high rates of catch-up saccades during eye tracking may be specific to schizophrenia. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in dorsal neck muscle activity related to imposed eye movement in the decerebrate pigeon

Movements of the head and eyes are known to be intimately related. Eye position has also been shown to be closely related to the electromyographic activity of dorsal neck muscles; however, extraocular muscle proprioception has not generally been considered to play a part in the control of such movements. We have previously shown that, in the pigeon, imposed movements of one eye modify the vestibular responses of several dorsal neck muscles in ways that are dependent on stimulus parameters such as the amplitude and velocity of imposed eye movement. The present study examines more closely the interactions between imposed eye movements and different muscle pairs. The three neck muscle pairs studied each responded to afferent signals from the extraocular muscles in discrete and specific ways which appeared to be correlated with their different actions. Complementary effects of imposed eye movements in the horizontal plane were seen for both the complexus and splenius muscle pairs, with imposed eye movements in one direction producing the largest inhibition of the ipsilateral muscle's vestibular response and imposed eye movements in the opposite direction the largest inhibition of the contralateral muscle's vestibular response. During roll tilt oscillation (ear-up/ear-down) in the frontal plane, similar complementary effects of imposed eye movement were seen in the complexus muscle pair, but the splenius muscle pair showed little tuning, with similar inhibition for imposed eye movement directed either upwards or downwards. In contrast to these complementary effects, the biventer cervicis muscle pair showed no vestibular modulation during vestibular stimulation in the horizontal plane and their spontaneous activity was not altered by imposed eye movement. During roll-tilt oscillation (ear-up/ear-down) in the frontal plane imposed eye movement directed vertically upwards increased both muscles' vestibular responses and imposed eye movement directed vertically downwards inhibited both muscles' vestibular responses. Section of the ophthalmic branch of the trigeminal nerve (deafferenting the eye muscles) abolished the effects of imposed eye movement on the neck muscle pairs. In conjunction with further control experiments these results provide compelling evidence that proprioceptive signals from the extraocular muscles reach the neck muscles and provide them with a functionally significant signal. We have previously shown that signals from the extraocular muscles appear to be involved in the control of the vestibulo-ocular reflex. It follows from the experiments reported here that proprioceptive signals from the extraocular muscles are also likely to be involved in the control of gaze.     

Ocular motor abnormalities in Huntington's disease

We review here the eye movements in patients with Huntington's disease (HD), concentrating upon saccades as they show the most prominent abnormalities. Inability to suppress reflexive glances to suddenly appearing novel visual stimuli and delayed initiation of voluntary saccades, including predictive saccades, are early and consistent findings. These two abnormalities can be interpreted in the context of a model, based upon the idea that the frontal lobes and basal ganglia contribute more to the control of voluntary than to reflexive types of saccades. Most patients eventually also show slow saccades but they are most prominent when the disease is early-onset. Slowing of saccades may reflect involvement of both the higher-level cerebral centers that trigger saccades and the areas in the brain stem that produce premotor saccade commands. The study of eye movements in HD has led to a fruitful interaction between basic science and clinical investigation, and has served as a paradigm for examining higher-level defects in saccadic eye movement control in patients with various degenerative, neurological diseases or with focal cerebral hemispheral lesions.     

Primate head-free saccade generator implements a desired (post-VOR) eye position command by anticipating intended head motion

Primate head-free saccade generator implements a desired (post-VOR) eye position command by anticipating intended head motion. J. Neurophysiol. 78: 2811-2816, 1997. When we glance between objects, the brain ultimately controls gaze direction in space. However, it is currently unclear how this is allocated into separate commands for eye and head movement. To determine the role of desired final eye position commands, and their coordination with intended head movement, we trained three monkeys to make large gaze shifts while wearing opaque goggles with a monocular 8 degrees aperture. Animals eventually developed a new set of context-dependent eye-head coordination strategies, in particular expanding the head range and compressing the eye-in-head range toward the aperture (while wearing the goggles). However, when we shifted the location of the aperture to a different subsection of the normal head-free oculomotor range (by covering the original aperture and creating a new one), eye-head saccades failed to acquire visual targets, because they continued to drive the eye ultimately toward the now occluded original aperture. Even when a head-stationary saccade acquired the new aperture, subsequent head-free saccades drove the eye eccentrically toward a point that anticipated the intended head movement, such that the subsequent vestibuloocular reflex slow phase brought the eye onto the location of the original aperture. Animals could only acquire the new aperture consistently after several days of retraining. These results suggest that 1) eye-head coordination is achieved by a plastic, context-dependent neural operator that uses information about initial eye/head position and intended movement to compute desired combinations of final eye/head position and 2) acquisition of these positions involves sophisticated anticipatory compensations for subsequent movement components, akin to those observed previously in complex oral and manual behaviors.     

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.     

Oculomotor testing in the differential diagnosis of degenerative ataxic disorders

BACKGROUND: Oculomotor abnormalities have been reported in patients with degenerative ataxic disorders. OBJECTIVE: To assess the diagnostic sensitivity and specificity of oculomotor deficits in patients with Friedreich ataxia (FA), cerebellar atrophy (CA), and olivopontocerebellar atrophy (OPCA). SETTING: Neurology clinic at a university hospital in Lübeck, Germany. PATIENTS: Seven patients with FA, 9 with CA, and 10 with OPCA were studied. These patients were selected from an ongoing follow-up study. MAIN OUTCOME MEASURES: Eye movements were recorded by electro-oculography; an extensive battery of quantitative tests was used. RESULTS: A proven CAG repeat expansion on chromosome 6 or 14 was significantly associated with reduced saccadic eye velocity and vertical gaze palsy (P<.001, Mann-Whitney U test). All 6 patients with OPCA and slow saccades had an autosomal-dominant inheritance; 4 of them were proved to have spinocerebellar atrophy type 1. In 9 of these patients (4 with FA, 1 with CA, and 4 with OPCA), the genetic defect could not be identified. Saccadic dysmetria, impairment of smooth pursuit and optokinetic nystagmus, deficient suppression of the vestibulo-ocular reflex by either visual or otolith input, and pathological nystagmus were attributed to degenerative lesions in different parts of the cerebellum. However, these symptoms failed to clearly distinguish between the different groups of patients, whereas decreased vestibulo-ocular reflex gain, slow saccades, and vertical gaze palsy pointed to an extracerebellar manifestation of the degenerative disease, occurring only in patients with OPCA and FA. CONCLUSIONS: In this prospective study, oculomotor disturbances were mainly related to cerebellar dysfunction. Only a few of them were caused by extracerebellar manifestations of the disease, such as slowing of saccades, which was characteristic for patients with OPCA of autosomal-dominant inheritance.     

Anticipatory saccades during smooth pursuit eye movements and familial transmission of schizophrenia

BACKGROUND: Smooth pursuit eye movement (SPEM) abnormalities are a putative marker of genetic risk for schizophrenia. Accurate SPEM performance requires the subject to activate neural systems responsible for smooth pursuit tracking, while simultaneously suppressing activity of neurons responsible for saccadic movements that would move the eye ahead of the target. This study examined whether specific aspects of SPEM dysfunction cosegregate with genetic risk in parents of schizophrenic probands. METHODS: Eighteen probands and their parents had SPEM recorded. Parents with an ancestral history of schizophrenia were hypothesized to be more likely than their spouses without such a history to carry a genetic risk for schizophrenia. RESULTS: Ten families had a single parent with a positive ancestral history for schizophrenia. The frequency of anticipatory saccades, which were mostly small, and the fraction of total eye movement that they represented were the only measures that differentiated the more likely genetic carrier parents in these families from their spouses and age-matched normals. CONCLUSIONS: Failure to suppress saccadic anticipation of target motion during smooth pursuit appears an aspect of SPEM dysfunction related to presumed genetic risk for schizophrenia.     

Evaluation of vestibular and visual oculomotor function

The visual system interacts synergistically with the vestibular system. A normally functioning vestibulo-ocular reflex is necessary but not sufficient for optimum visual acuity during head motion. Studies of dynamic visual acuity, the acuity achieved during relative motion of visual targets or of the observer, indicate that motion of images on the retina markedly compromises vision. The vestibulo-ocular reflex normally provides a substantial measure of stabilization of the retina during head movements, but purely vestibular compensatory eye movements are not sufficiently precise for optimal vision under all circumstances. Other mechanisms, including visual tracking, motor preprogramming, prediction, and mental set, interact synergistically to optimize the gain (eye velocity divided by head velocity) of compensatory head movements. All of these mechanisms are limited in their capacity to produce effective visual-vestibular interaction at higher rotational frequencies and velocities. It is under these conditions that vestibular deficits give rise to symptoms of oscillopsia. Patients having vestibular lesions exploit mechanisms of visual-vestibular interaction to compensate by substitution for deficient vestibular function. Thus, for accurate topographic clinical diagnosis of vestibular lesions, testing conditions should isolate purely vestibular responses. This may be done by testing reflex eye movements during passively generated rotations in darkness, or perhaps by testing during other types of motion under conditions of extreme frequency and velocity sufficient to attenuate the effects of visual-vestibular interaction. This article reviews clinical tests of vestibular function in relation to synergistic interactions with vision.     

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)     

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.     

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.