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Biomedical subjects

A F Fuchs

Publications and source records attributed to A F Fuchs.

At least 37 records · Page 2Linked to original sources
PubMed1997

Smooth pursuit in 1- to 4-month-old human infants.

The ability of human infants < or = 4 months of age to pursue objects smoothly with their eyes was assessed by presenting small target spots moving with hold-ramp-hold trajectories at ramp velocities of 4-32 deg/sec. Infants as young as 1 month old followed such target motions with a combination of smooth-pursuit and saccadic eye movements interrupted occasionally by periods when the eyes remained stationary. The slowest targets produced variable performance, but targets moving 8-32 deg/sec produced consistent pursuit behavior, even in the youngest infants. By the fourth month, eye-movement latency decreased and smooth-pursuit gain and the percentage of smooth pursuit per trial increased for all target velocities, though these measures had not yet reached adult levels.

Aging↗
PubMed1997

Response properties of pretectal omnidirectional pause neurons in the behaving primate.

We have identified a region in the pretectum of rhesus monkeys (Macaca mulatta) that contains units that evince a complete cessation in firing immediately after saccades. The pause occurs for saccades to target steps and catch up saccades during smooth pursuit, spontaneously in complete darkness or after quick phases of nystagmus. Because the pause in unit firing always follows saccade onset, we call these neurons following omnidirectional pause neurons (FOPNs). Because the pause also occurs with saccades in the dark, it is related to the saccade per se and is not a visually contingent response. The duration of the pause in firing exceeded the duration of all saccades up to 40 deg. For targeting saccades, the start of the pause was locked rather tightly to the beginning of the saccade but began an average of 51 ms after the saccade did. The end of the pause was linked only loosely to either the beginning or end of the saccade. About half (54%) of our 59 FOPNs also discharged a distinct burst of firing that preceded the pause. In different units, the burst preceded saccade onset by from 0 to 20 ms with an average of 11 ms and therefore could signal the occurrence of an impending saccade. The presaccadic burst was not correlated with any parameter of the saccade. Most FOPNs were found 278 microns, on average, dorsal to the direction-selective units characteristic of the pretectal nucleus of the optic tract (NOT) and occasionally slightly beyond the anterior-posterior and medial-lateral borders of the NOT. The FOPN region does not coincide with any known anatomically or functionally delineated pretectal nucleus. Because the characteristics of the FOPN pause are not reflected in the characteristics of the saccade and the FOPN pause occurs well after the saccade is over, it is unlikely that the pause in pretectal FOPNs is involved with saccade generation. On the other hand, the leading burst exhibited by the majority of FOPNs reliably signals that a saccade is occurring but neither its size nor direction. Perhaps this signal indicating the occurrence of all saccades is routed to visual relay neurons to effect saccadic modification of visual pathways. The substantial efferent connections of the FOPN/NOT region to the pregeniculate nucleus and the saccadic discharge or pregeniculate cells are discussed in the context of this suggestion.

Action Potentials↗
PubMed1997

Characteristics of saccadic gain adaptation in rhesus macaques.

We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15 degrees and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate.

Adaptation, Physiological↗
PubMed1997

Participation of caudal fastigial nucleus in smooth pursuit eye movements. II. Effects of muscimol inactivation.

We studied the effect of temporarily inactivating the caudal fastigial nucleus (CFN) in three rhesus macaques trained to make smooth pursuit eye movements. We injected the gamma-aminobutyric acid A agonist muscimol into one or both CFNs where we had recorded pursuit-related neurons a few minutes earlier. Inactivating the CFN on one side impaired pursuit in one monkey so severely that it could not follow step-ramp targets moving at 20 degrees/s, the target velocity that we used to test the other two monkeys. We tested this monkey with targets moving at 10 degrees/s. In all three monkeys, unilateral CFN inactivation either increased the acceleration of ipsilateral step-ramp pursuit (in 2 monkeys, to 144 and 220% of normal) or decreased the acceleration of contralateral pursuit (in 1 monkey, to 71% of normal). Muscimol injected into both CFNs in two of the monkeys left both ipsilateral and contralateral acceleration nearly normal in both monkeys (101% of normal). Unilateral CFN inactivation also impaired the velocity of maintained pursuit as the monkeys tracked a target moving at a constant velocity or oscillating sinusoidally. Averaged across both types of movements in all three monkeys, gains for ipsilateral, contralateral, upward, and downward pursuit were 94, 67, 84, and 73% of normal, respectively. Unilateral CFN inactivation also impaired the monkeys' ability to suppress their vestibuloocular reflex (VOR). Averaged across the two monkeys VOR gain during suppression increased from 0.06 to 0.25 during yaw rotation and from 0.21 to 0.59 during pitch rotation. Bilateral CFN inactivation reduced pursuit gains in all directions more than unilateral injection did. In the two monkeys tested, ipsilateral, contralateral, upward, and downward gains went from 94, 86, 85, and 74% of normal, respectively, after we inactivated one CFN to 88, 73, 80, and 64% of normal after we also inactivated the second CFN. We can explain many, but not all, of the effects of CFN activation on smooth pursuit with the behavior of CFN neurons, and the assumption that the activity of each CFN neuron helps drive pursuit movements in the direction that best activates that neuron. We conclude that the CFN, like the flocculus-ventral paraflocculus, is a cerebellar region involved in control of smooth pursuit.

Animals↗
PubMed1997

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.

Acclimatization↗
PubMed1997

Decrease in saccadic performance after many visually guided saccadic eye movements in monkeys.

PURPOSE: To investigate the influence of repeated saccades and of background illumination on the metrics and dynamics of visually guided targeting saccades. METHODS: Eye movements were measured by magnetic search coil technique in seven trained monkeys (Macaca mulatta) while they performed many visually guided saccades in the dark or in dim background light. RESULTS: After 2000 to 7000 saccades in the dark, peak eye velocity on the average decreased by 20%, saccadic gain decreased slightly by 4.5%, and saccadic latency increased by 15%. All parameters also showed increased variability. In contrast, when testing was done in dim light, there was little to no change in average saccadic metrics and latency. CONCLUSIONS: The changes in saccadic metrics and dynamics in the dark do not reflect a change of the ocular plant but may reflect a change in the cortical or cerebellar influences on the brain stem burst generator linked to the monkeys attentional state. Background light mostly prevents this change.

Adaptation, Ocular↗
PubMed1996

Transfer of gain changes from targeting to other types of saccade in the monkey: constraints on possible sites of saccadic gain adaptation.

1. Our goal was to use behavioral experiments to delimit where in the simian oculomotor system the gain of horizontal saccadic eye movements might be controlled. Our strategy was to change the gain of saccades to visual target steps (called targeting saccades) and to examine whether these changes transferred to other types of saccades. We reduced the gain of targeting saccades by jumping the target backward as a saccade was made so that the saccade appeared to overshoot. After 1,000-1,500 saccades to such backstepping targets, the average overshoot, and therefore the saccadic gain, had decreased substantially. 2. After the gain of targeting saccades had been reduced by 15-22%, several kinds of saccades were tested. Most were elicited by various visual targets. Some were made to jumping targets, which were timed to elicit saccades with longer (delayed saccades) or shorter (express saccades) latencies than normal or to targets that disappeared after a brief exposure (memory-guided saccades). Others were elicited to stationary targets (self-paced saccades) or in pursuit of a smoothly moving target (catchup saccades). Finally, we tested the saccadic fast phases of vestibular and optokinetic nystagmus. 3. Gain reduction of targeting saccades transferred at least partially to all the other types of saccades made to target jumps. The percentage gain transfer was calculated as (gain reduction of test saccades)/(gain reduction of adapted targeting saccades). The average percent transfer to delayed, memory-guided, and express saccades was 96, 88, and 91%, respectively. 4. Monkeys also showed substantial gain transfer to self-paced saccades, which scanned stationary targets. The average percentage gain transfer was 69% in the four animals tested. When two humans performed the same task, there was no transfer at all. These data suggest that saccadic gain adjustment involves different processes in monkeys and humans. 5. The transfer of gain to the catchup saccades of smooth pursuit varied from 41 to 100% across the four monkeys tested. Nevertheless, the average percentage gain transfer for all the animals was 75%. 6. As judged by the amplitude distribution of fast phases before and after adaptation, there was little, if any, saccadic gain transfer to the fast phases of vestibular or optokinetic nystagmus. In 12 of 13 experiments, there was no significant decrease in fast phase amplitude after a gain reduction of targeting saccades (P > 0.1). 7. This study shows that the average percentage gain transfer from targeting to delayed, express, memory-guided, self-paced, and catchup saccades was never < 69%. Although there was substantial transfer to saccades elicited by jumping, stationary, remembered, or slowly moving visual targets, there was relatively little to the saccadelike fast phases of nystagmus. The transfer of saccadic gain to the very short-latency express saccades suggests that adaptation modifies a subcortical locus. Moreover, the major locus must lie only in the premotor pathway for visual saccades, because saccadic gain adaptation is only poorly transferred to the fast phases of vestibular and optokinetic nystagmus.

Adaptation, Physiological↗
PubMed1996

Hair cell regeneration and recovery of the vestibuloocular reflex in the avian vestibular system.

1. Although auditory and vestibular hair cells are known to regenerate after aminoglycoside intoxication in birds, there is only sparse evidence that the regenerated hair cells are functional. To address this issue, we examined the relation of hair cell regeneration to recovery of the vestibuloocular reflex (VOR), whose afferent signal originates at hair cells in the vestibular epithelium. Hair cell damage was produced by treating white Leghorn chicks (Gallus domesticus, 4-8 days posthatch) with streptomycin sulfate in normal saline (1,200 mg.kg-1.day-1 im) for 5 days. 2. In the 1st wk after treatment, the VOR gain was essentially 0, and hair cell density as assessed by light microscopy was approximately 40% of normal. Between the 1st and 3rd wk after treatment, the VOR was present. Although VOR gain varied considerably from one chick to another, it increased, on average, between the 1st and 3rd wk, as did the average hair cell density. At the end of 8-9 wk, the gain and phase of the VOR had returned to normal values, as had the average density of hair cells. 3. Therefore, despite the catastrophic initial effect of hair cell loss on the VOR, recovered hair cells appeared to restore the VOR completely. Average hair cell density increased with average VOR gain. VOR gain correlated better with recovery of type 1 hair cells than with recovery of type II hair cells. 4. In contrast to hair cell density, the appearance of the vestibular epithelia as assessed by hair cell stereocilia in scanning electron micrographs was a poor indicator of VOR gain. In both treated and control birds, epithelia with the same appearance could have quite different VOR gains, suggesting a variation in the functional viability of the hair cells. 5. This observation suggests that several factors, such as the repair of stereocilia, the efficacy of hair cell synapses on afferent fibers, and the extent of compensation by central vestibular pathways, may affect the recovery of VOR gain. However, our data suggest that hair cell regeneration plays an important role in this recovery.

Animals↗
PubMed1995

Rapid horizontal gaze movement in the monkey.

1. We studied horizontal eye and head movements in three monkeys that were trained to direct their gaze (eye position in space) toward jumping targets while their heads were both fixed and free to rotate about a vertical axis. We considered all gaze movements that traveled > or = 80% of the distance to the new visual target. 2. The relative contributions and metrics of eye and head movements to the gaze shift varied considerably from animal to animal and even within animals. Head movements could be initiated early or late and could be large or small. The eye movements of some monkeys showed a consistent decrease in velocity as the head accelerated, whereas others did not. Although all gaze shifts were hypometric, they were more hypometric in some monkeys than in others. Nevertheless, certain features of the gaze shift were identifiable in all monkeys. To identify those we analyzed gaze, eye in head position, and head position, and their velocities at three points in time during the gaze shift: 1) when the eye had completed its initial rotation toward the target, 2) when the initial gaze shift had landed, and 3) when the head movement was finished. 3. For small gaze shifts (< 20 degrees) the initial gaze movement consisted entirely of an eye movement because the head did not move. As gaze shifts became larger, the eye movement contribution saturated at approximately 30 degrees and the head movement contributed increasingly to the initial gaze movement. For the largest gaze shifts, the eye usually began counterrolling or remained stable in the orbit before gaze landed. During the interval between eye and gaze end, the head alone carried gaze to completion. Finally, when the head movement landed, it was almost aimed at the target and the eye had returned to within 10 +/- 7 degrees, mean +/- SD, of straight ahead. Between the end of the gaze shift and the end of the head movement, gaze remained stable in space or a small correction saccade occurred. 4. Gaze movements < 20 degrees landed accurately on target whether the head was fixed or free. For larger target movements, both head-free and head-fixed gaze shifts became increasingly hypometric. Head-free gaze shifts were more accurate, on average, but also more variable. This suggests that gaze is controlled in a different way with the head free. For target amplitudes < 60 degrees, head position was hypometric but the error was rather constant at approximately 10 degrees.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Anatomical connections of the primate pretectal nucleus of the optic tract.

The pretectal nucleus of the optic tract (NOT) plays an essential role in optokinetic nystagmus, the reflexive movements of the eyes to motion of the entire visual scene. To determine how the NOT can influence structures that move the eyes, we injected it with lectin-conjugated horseradish peroxidase and characterized its afferent and efferent connections. The NOT sent its heaviest projection to the caudal half of the ipsilateral dorsal cap of Kooy in the inferior olive. The rostral dorsal cap was free of labeling. The NOT sent lighter, but consistent, projections to other visual and oculomotor-related areas including, from rostral to caudal, the ipsilateral pregeniculate nucleus, the contralateral NOT, the lateral and medial terminal nuclei of the accessory optic system bilaterally, the ipsilateral dorsolateral pontine nucleus, the ipsilateral nucleus prepositus hypoglossi, and the ipsilateral medial vestibular nucleus. The NOT received input from the contralateral NOT, the lateral terminal nuclei bilaterally, and the ipsilateral pregeniculate nucleus. Although our injections involved the pretectal olivary nucleus (PON), there was neither orthograde nor retrograde labeling in the contralateral PON. Our results indicate that the NOT can influence brainstem preoculomotor pathways both directly through the medial vestibular nucleus and nucleus prepositus hypoglossi and indirectly through both climbing and mossy fiber pathways to the cerebellar flocculus. In addition, the NOT communicates strongly with other retino-recipient zones, whose neurons are driven by either horizontal (contralateral NOT) or vertical (medial and lateral terminal nuclei) fullfield image motion.

Animals↗
PubMed1994

Coordination of gaze shifts in primates: brainstem inputs to neck and extraocular motoneuron pools.

To determine whether there are brainstem regions that provide common input to the motoneurons that move both the head and the eyes, we injected wheat germ agglutinin-horseradish peroxidase complex (WGA-HRP) into neck motoneuron pools at spinal level C2 (N = 3) and extraocular motoneuron pools in the abducens (N = 1) and oculomotor/trochlear (N = 1) nuclei of rhesus and fascicularis macaques. We also injected WGA-HRP into spinal level C5-7 (N = 1) of a fascicularis macaque for comparison. After injections into C2, we observed retrogradely labeled cells in the ventral reticular formation (NRV), the gigantocellular reticular formation (NRG), and both the oral (NRPO) and the caudal (NRPC) divisions of the paramedian pontine reticular formation (PPRF). There was also a column of labeled cells in the cuneate reticular nucleus (NCUN) just lateral to the ipsilateral periaqueductal gray (PAG). This column extended rostrally into the central mesencephalic reticular formation (CMRF). In addition, there were labeled cells in the region ventral and caudal to the rostral interstitial nucleus of the MLF (riMLF), the area lateral to the interstitial nucleus of Cajal (INC), and the ventral part of the lateral vestibular nucleus (LVN) and lateral part of the medial vestibular nucleus (MVN). There were also a few labeled cells in the fastigial (FN) and interposed (IN) nuclei of the cerebellum but very few in the superior colliculus (SC). In contrast, the injection into C5-7 labeled many cells in the lateral vestibular nucleus (LVN) and very few in FN or IN. Injecting WGA-HRP into the abducens nucleus and the surrounding tissue labeled many cells in SC, PPRF, MVN, FN, and nucleus prepositus hypoglossi (NPH). Injecting into the oculomotor/trochlear nuclei and nearby tissue labeled cells in SC, INC, riMLF, FN, IN, MVN, and superior vestibular nucleus (SVN). Structures that project to both neck and eye motoneuron pools, and therefore probably participate in both head and eye movements, include the lateral part of the MVN and both NRPO and NRPC in the PPRF. Those that project primarily to neck motoneurons in C2 include the NRV, the NRG, and the NCUN-CMRF column. Those projecting exclusively to extraocular nuclei include the NPH, INC, riMLF, NRPD, and SC. We use these data to propose a scheme for control of combined eye-head movements in monkeys.

Afferent Pathways↗
PubMed1994

Participation of the caudal fastigial nucleus in smooth-pursuit eye movements. I. Neuronal activity.

1. We recorded single-unit activity from neurons of an output of the cerebellum, the fastigial nucleus, in two rhesus macaques while the monkeys tracked small moving targets with their eyes. Many neurons in the caudal part of the fastigial nucleus exhibited a modulation in their discharge rates when smooth-pursuit eye movements were elicited by either sinusoidal or step-ramp motions of a small target. 2. The pursuit direction that elicited the most vigorous modulation in unit firing to sinusoidal target motion could be horizontal, vertical, or oblique. Most often, the preferred direction was in the contralateral and/or downward direction (50 of 69 neurons) or in the ipsilateral and/or upward direction (13 of 69). 3. For units whose preferred smooth-pursuit directions were either contralateral/downward or ipsilateral/upward during sinusoidal pursuit, peak firing as measured by the phase shift of periodic modulation at 0.5-0.8 Hz occurred near the time of peak velocity. The discharge of 80% of the neurons with contralateral/downward preferred directions preceded eye velocity by an average of -27 degrees; thus these neurons discharged maximally during eye acceleration. In contrast, neurons with ipsilateral/upward preferred directions lagged peak velocity by an average of +10.5 degrees and therefore discharged during eye deceleration. 4. The average eye velocity sensitivity for sinusoidal pursuit between 0.5 and 0.8 Hz was 0.83 +/- 0.57 (SD) spikes/s per degrees/s. We also tested 36 units during pursuit at a variety of frequencies in their preferred directions and found that firing rates increased monotonically with peak eye velocity. However, the firing rate saturated at velocities ranging from 20 to 60 degrees/s for different units. 5. When a monkey tracked a step-ramp target motion, three discharge patterns emerged in the 27 units tested. Just over half of the units discharged a burst of spikes that preceded (average lead of 27.4 +/- 17 ms) and lasted throughout the initial third of the eye acceleration; the burst was followed by a subsequent steady firing that continued after the eye had accelerated to its steady velocity. Fewer neurons discharged a burst that began late in the acceleration and was followed by steady firing. Occasional neurons showed only a gradual increase in firing rate during acceleration followed by a steady discharge. 6. Thirty of the 31 fastigial smooth-pursuit units tested also were modulated during sinusoidal yaw and/or pitch oscillations while the animals fixated a spot that rotated with them.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

Role of the caudal fastigial nucleus in saccade generation. I. Neuronal discharge pattern.

1. The effects of lesions in both human and nonhuman primates have implicated the cerebellum in the control of rapid eye movements, i.e., saccades. To examine the neural substrate of this control, we recorded the discharge patterns of cerebellar output cells in the fastigial nucleus while monkeys tracked a small, jumping spot of light. 2. In the caudal fastigial nucleus, neurons discharged for saccades in one or several directions. All exhibited a burst. Some also exhibited a saccade-related pause in firing either before or after saccades greater than approximately 3-5 degrees. Thirty-seven percent discharged only a burst, 44% also exhibited a pause before bursts in certain directions, and 19% also paused after the saccade-related burst in certain directions. Although many cells discharged steadily during intersaccadic intervals, few exhibited a robust relation between firing rate and eye position. 3. As a measure of directional selectivity, we plotted the burst lead time as a function of saccade direction for saccades of similar (10 degrees) radial amplitudes. Of 20 neurons tested, 17 burst earliest for contralateral saccades and 1 for upward saccades; 2 others showed little dependence on direction. Of 19 additional units tested only in the horizontal direction, 18 burst earlier for contralateral saccades. 4. For contralateral saccades the burst preceded saccades of all sizes by at least 7.7 ms on average. For ipsilateral saccades, the burst preceded small saccades by an average of 10.3 ms. However, as ipsilateral saccade size increased, the burst began later and later relative to saccade onset so that, on average, it always occurred after the onset of 20 degrees saccades but well before the saccade ended. 5. Many fastigial saccade-related units showed increases in the number of spikes with saccade size and in burst duration with saccade duration in one or more directions. For either relation the highest average correlation coefficients ranged from 0.6 to 0.65. In general, the average correlation coefficients and slopes for either relation were slightly larger for contralateral saccades. Pure burst neurons did not display better average correlations than neurons that also paused. For neurons that also paused either before or after saccades, there was a weak tendency for pause duration to increase with the duration of larger saccades. 6. We tested the effect of eye position on unit discharge in 13 cells by requiring the monkey to make 10 degrees ipsilateral and contralateral saccades from a variety of starting positions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation.

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗