Department of Biological Structure and Regional Primate Research Center, University of Washington, Seattle, Washington 98195-7420
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ABSTRACT |
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Robinson, Farrel R.. Role of the Cerebellar Posterior Interpositus Nucleus in Saccades I. Effect of Temporary Lesions. J. Neurophysiol. 84: 1289-1302, 2000. The ventrolateral corner of the cerebellar posterior interpositus nucleus (VPIN) contains many neurons that respond during saccades. To characterize the VPIN contribution to saccades, I located this area in three monkeys with single-unit recording and injected the GABAA agonist muscimol among saccade-related neurons there to reduce or eliminate neural activity. I compared the size, direction, velocity, and duration of saccades recorded before and after a unilateral injection in all three monkeys. In two of three monkeys, I also examined saccades after bilateral injection. After unilateral VPIN inactivation, upward saccades were abnormally large (avg. across all 3 monkeys = 112% of normal) and downward saccades were abnormally small (avg. across all 3 monkeys = 94% of normal). In the two monkeys tested, bilateral inactivation increased these abnormalities. Upward saccades went from 111% of normal size in these two monkeys after unilateral inactivation to 120% after bilateral inactivation; downward saccades went from 97 to 86%. VPIN inactivation caused changes in saccade gain and did not add of a constant offset to saccades. (The 1 exception was upward saccades in 1 monkey in which both gain and offset changed.) Neither uni- nor bilateral VPIN inactivation consistently affected the size of horizontal saccades (uni- avg. = 101% normal; bi- avg. = 97% normal). In two of the three monkeys, saccades to horizontal targets angled significantly upward after VPIN inactivation (uni- avg. = 3.6° above normal, bi- avg. = 10.3° above normal). The velocities of horizontal saccades were not strongly affected, but downward saccades exhibited abnormally low peak velocities and long durations. Upward velocities were inconsistently changed. I interpret these results to mean that the activity of some VPIN neurons helps drive the eyes downward and the activity of others helps drive the eyes upward. The downward drive outweighs the upward drive. The net effect of VPIN inactivation is to deprive all saccades of a downward component and to slow downward saccades.
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INTRODUCTION |
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Cerebellar damage disrupts
saccades in humans (e.g., Selhorst et al. 1976) and
monkeys (e.g., Ritchie 1976
). Anatomical and recording
studies to date indicate that there are two parts of the cerebellar
nuclei that participate in saccades: the caudal fastigial nucleus
(CFN), also called the fastigial oculomotor region (e.g.,
Ohtsuka and Noda 1990
), and the ventrolateral corner of
the posterior interpositus nucleus (VPIN).
Both the CFN and VPIN are positioned to receive eye-movement-related
input and to influence saccades. The CFN receives descending saccade-related input via relays in the pontine nuclei from the frontal
eye field, the supplementary eye field, and the superior colliculus.
The frontal eye field (Stanton et al. 1988) and the supplementary eye field (Shook et al. 1990
) project to
the nucleus reticularis tegmenti pontis (NRTP). The superior colliculus
(Harting 1977
) projects to the dorsolateral pontine
nucleus (DLPN). The NRTP and DLPN both project to the CFN (Noda
et al. 1990
) and to lobules VI and VII of the cerebellar cortex
in the posterior vermis (Yamada and Noda 1987
). These
lobules, sometimes called the oculomotor vermis, project to the CFN
(Yamada and Noda 1987
). Activity in CFN neurons can
influence saccades via CFN efferent connections to regions of the brain
stem associated with three elements of the burst generator for
horizontal saccades: inhibitory burst neurons, excitatory burst
neurons, and omnipause neurons (Noda et al. 1990
;
Scudder 1997
).
Like the CFN, the VPIN receives saccade-related input from the pontine
nuclei. The DLPN projects heavily to a large, laterally placed part of
the cerebellar cortex, the dorsal paraflocculus (Glickstein et
al. 1994). This part of the cortex, in turn, sends a large
projection to the VPIN (Swales et al. 1997
).
VPIN efferents terminate in two regions through which they could
influence saccades. One is the contralateral superior colliculus, in
which VPIN axons terminate throughout much of the intermediate layers
(May et al. 1990). The other is a projection to the
contralateral interstitial nucleus of Cajal (INC), though this
projection may be small (May et al. 1992
). The INC
projects to the oculomotor and trochlear nuclei (Kokkoroyannis
et al. 1996
; Steiger and Büttner-Ennever 1979
), and INC activity is critical to vertical saccades
(Fukushima and Fukushima 1992
; Helmchen et al.
1996
).
Consistent with their anatomical connections, the CFN and VPIN both
contain neurons that modulate their activity during saccades. CFN
neurons discharge a burst of action potentials for nearly every
saccade, whatever its size or direction (Fuchs et al.
1993; Ohtsuka and Noda 1991
). This activity is
clearly important for the production of normal saccades; when it is
reduced or eliminated by muscimol injections, saccades become dysmetric
and abnormally slow and variable (Robinson et al. 1993
).
VPIN neurons also discharge a burst of action potentials for nearly
every saccade. Saccade-related VPIN responses were first described in a
study of limb movement-related responses in the interpositus nuclei of
the monkey cerebellum (van Kan et al. 1993). This work
used observations from video tapes to document the existence of a
distinct region of eye-movement-related neurons in the VPIN. It did
not, however, measure eye movements and so did not characterize the
relation between eye movement metrics and neural responses.
Why are there two separate regions in the cerebellar nuclei (the CFN
and VPIN) containing neurons that burst vigorously during nearly every
saccade? To answer this question, we need to know what each region
contributes to saccades. The role of the CFN has been studied and
modeled (e.g., Dean 1995; Lefévre
1998
), but to date we know little about the role of the VPIN.
To investigate the role of the VPIN in saccades, I compared saccades
made by monkeys before and after I injected muscimol among
saccade-related neurons there. The results are presented in this
article. A subsequent paper will describe the data obtained when VPIN
neurons were recorded while the monkeys made a variety of saccades
(F. R. Robinson, A. F. Fuchs, and A. Straube, unpublished data). Preliminary results from both the inactivation and recording studies of the VPIN have been reported in an abstract (Robinson et al. 1996).
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METHODS |
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Animal preparation
Subjects were three adolescent male rhesus macaques
(Macaca mulatta), monkeys 1, 2, and
3. In sterile surgery under general anesthesia, each monkey
was implanted with three turns of fine Teflon-coated wire around one
eye and acrylic lugs used to stabilize the head during experiments
(Fuchs and Robinson 1966). A recording chamber was
implanted over a small hole cut through the skull. The chamber was
centered with a stereotaxic apparatus on the midline 8 mm posterior to
ear bar zero and pointed directly downward.
I recorded eye movements with the search coil technique
(Robinson 1963) and trained the monkeys with applesauce
reward to foveate a small (0.3°) spot of light and to track the
spot's movements with saccades. The target spot was projected onto a
screen 57 cm in front of the monkey via two galvanometers that allowed
a computer to control the spot's horizontal and vertical positions.
All surgical and behavioral training procedures were approved by the Animal Care and Use Committee at the University of Washington. The animals were cared for by the veterinary staff of the Regional Primate Research Center. They were housed under conditions that comply with National Institutes of Health standards as stated in the Guide for the Care and Use of Laboratory Animals (DHEW Publication NIH85-23, 1985) and with recommendations from the Institute of Laboratory Animal Resources and the American Association for Accreditation of Laboratory Animal Care.
Locating the VPIN
To find the VPIN, I first located the CFN 1-2 mm lateral to the midline, near the anterior-posterior center of the chamber, and ~25 mm below the surface of the brain. It was identifiable by the characteristic bursting of many of its neurons during saccades. The VPIN was located ~4 mm lateral to the CFN and ~2 mm more ventral. It too was identifiable by the saccade-related bursts of its neurons. I made small electrolytic lesions at the sites of some eye-movement-related neurons in the VPIN by passing of 30 µA for 30 s (electrode positive) through the recording electrode.
Injecting muscimol
I mapped the position of saccade-related neurons in the VPIN
with several electrode penetrations and injected muscimol into the
center of this region. I recorded single-unit activity with epoxy-coated tungsten electrodes and standard amplification and filtering. Once single-unit activity confirmed the presence of saccade-related activity at the intended injection site, I withdrew the
electrode and replaced it with an injection pipette. The pipette consisted of a length of 32-gauge hypodermic tubing with a pulled-glass micropipette tip (ID 25 µm) glued over one end. Several feet of
polyethylene tubing connected a solenoid valve to the other end of the
hypodermic tubing. The pipette and several centimeters of the connected
tube were filled with a solution consisting of 1 mg/ml (8.75 mM)
muscimol in normal saline. The pipette was inserted in the same guide
tube that was used for the recording, and its tip was advanced to the
dorsal-ventral center of the region from which saccade-related activity
had just been recorded. The muscimol solution was injected with the use
of a solenoid valve system (WPI PV830), which delivered a number of
brief (~15 ms) air pressure pulses to move the meniscus a calibrated
distance down the tube. With the aid of a ×50 microscope to view the
meniscus, injected volumes could be resolved to within ~10 nl. The
injections took 5-20 min. The pipette was left in place for 5 min
after each injection and then withdrawn.
Monkey 1 received a 1-µl injection into its left VPIN. Monkey 2 received a 1-µl injection into its right VPIN and then, ~30 min later, after I recorded a variety of saccades, I made a second 1-µl injection into its left VPIN, and then recorded more saccades. This procedure allowed me to evaluate the effects of both unilateral and bilateral VPIN inactivation. Monkey 3 also received two injections but in reverse order, i.e., first into the left VPIN and then into the right.
Data collection and analysis
Before each injection in each monkey I recorded normal horizontal and vertical saccades while it tracked the target spot jumping from one position to another. In monkey 1, I recorded horizontal and vertical saccades to targets 10 and 20° from the center of gaze (centrifugal saccades) and back to the center of gaze (centripetal saccades). In monkeys 2 and 3, I recorded these saccades as well as horizontal and vertical saccades tracking target steps of other sizes ranging from 2 to 30°.
Within ~10 min of the end of an injection, its oculomotor effects were evident, most noticeably as an increase in the number and size of corrective saccades after vertical saccades. Starting then, I recorded saccades to the same type of preinjection target steps presented before the injection. The effects of the muscimol injection were still clear, with no apparent changes, when recording was stopped 1.5-2 h after the injection. There were no abnormalities in the monkeys' eye movements during recording on the day after the injection. Analog voltages corresponding to the monkeys' horizontal and vertical eye positions and horizontal and vertical target positions were recorded on videotape with a PCM recording adapter (Vetter 4000A). Eye and target records were digitized from the videotape at 1 kHz. A custom saccade analysis program measured saccade gain, velocities, latencies, and durations and displayed the trajectories of selected saccades. The program smoothed eye velocity with a moving 3-point average thus introducing a maximum delay in the constructed velocity record of 3 ms. For analysis, saccades began when eye velocity exceeded 20°/s and ended when it fell <20°/s. Eye acceleration was the average change in eye velocity between the saccade start and the point of peak velocity; deceleration was the average change in eye velocity between peak velocity and saccade end. Acceleration duration was the interval between saccade start and the point of peak velocity; deceleration duration was the interval between peak velocity and saccade end. Saccade latency was the difference between the time the target moved to a new location and saccade start.
I used a simple ANOVA with the Bonferroni correction for repeated tests to compare averages of measurements before and after injections. I used a t-test for the difference in slopes to compare data fit with lines. For both comparisons, I considered P < 0.05 to be significant.
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RESULTS |
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Neurons with saccade-related bursts were located in a region extending ~1 mm medial-lateral, ~1 mm anterior posterior, and centered ~4 mm lateral to the eye-movement-related part of the CFN. Marking lesions confirmed that this small eye-movement-related region was in the VPIN (Fig. 1).
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Saccade size and direction
In each monkey, VPIN inactivation caused vertical saccades to end above their targets. Upward saccades became too large and downward saccades became too small. In addition, in monkeys 1 and 2, leftward and rightward saccades angled upward from horizontal to end above their targets. About 200 ms after each saccade that ended above its target, the monkey made downward corrective saccades to foveate the target. Often several corrective saccades were necessary because the hypometria of downward saccades made the first, and sometimes the second, corrective saccade fall short.
Figure 2 shows the effect of VPIN inactivation in monkey 2 on the trajectories of saccades to 10° target displacements. Bilateral inactivation made saccades in all four directions end above their targets by changing the size of vertical saccades and the direction of horizontal saccades (Fig. 2C). Inactivating only the right VPIN caused smaller changes in the size of vertical saccades and the direction of horizontal saccades (Fig. 2B). I measured the changes caused in saccade size and saccade direction in all three monkeys.
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SACCADE SIZE. I measured the size of a saccade as gain, i.e., the size of a saccade divided by the distance to the target. VPIN inactivation caused no consistent effect on the gain of horizontal saccades to 10° target displacements (Fig. 3, A and B). For example, inactivating the left VPIN slightly decreased the gain of right centrifugal saccades in monkey 1 but slightly increased the gain of these same saccades in monkey 3. All three monkeys exhibited a significant increase in the gain of upward saccades and a significant decrease in the gain of downward saccades after VPIN inactivation (Fig. 3, C and D), although the pattern of gain changes was slightly different in each monkey.
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GAIN OR OFFSET?
In the preceding text, I describe the overshoot in upward saccades and
the undershoot of downward saccades after VPIN inactivation as a gain
change. However, it is also possible that the dysmetria of vertical
saccades reflects a constant upward offset added to the end position of
each vertical saccade. This is plausible because data from cat gaze
movements (Goffart and Pelisson 1994) and preliminary results from monkey saccades (Goffart and Sparks 1996
)
indicate that changes in the offset of saccade end position, not
changes in saccade gain, account for the overshoot of ipsilateral
saccades after unilateral inactivation of the CFN.
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SACCADE DIRECTION. Figure 5 shows the average error in the direction of saccades to 10° horizontal and vertical target displacements before and after VPIN inactivation. Direction errors are expressed as the differences in degrees between saccade and target directions. For example, monkey 1's centrifugal rightward saccades normally ended an average of ~1.4° below the target but, after inactivation of the left VPIN, ended an average of ~4.7° above the target (Fig. 5A, left). Unilateral VPIN inactivation in both monkeys 1 and 2 caused both leftward and rightward (i.e., both ipsiversive and contraversive) saccades to end significantly above their normal end positions. The subsequent bilateral VPIN inactivation in monkey 2 caused a further significant increase in the upward angle of its horizontal saccades (Fig. 5, A and B, middle). VPIN inactivation had no consistent effect on the direction error of monkey 3's horizontal saccades. Inactivation of monkey 3's left VPIN caused rightward (contraversive) saccades to end significantly lower than normal (Fig. 5, A and B, right). Subsequent inactivation of the other VPIN caused most leftward and rightward saccades to end near normal. An exception was leftward centrifugal saccades which ended significantly above their normal end position.
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Saccade velocity
EYE VELOCITY PROFILES. Figure 6 shows average eye velocity profiles of saccades to 10° target displacements before and after VPIN inactivation. The numbers in Table 2 are the percent of normal values exhibited by saccades after VPIN inactivation, i.e., 100 represents a postinactivation value the same as normal, 200 is twice normal, and 50 is half normal.
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ARE SACCADES AFTER VPIN INACTIVATION ON THE MAIN SEQUENCE?
All of the saccades in Fig. 6 and Table 2 were to 10° target
displacements. As the data in Fig. 2 shows, vertical saccades to 10°
target displacements were often larger or smaller than 10°. It is
possible that the velocity profiles of saccades after VPIN inactivation
are abnormal simply because the saccades were not their normal size.
This seems unlikely from the information in Figs. 3 and 6. Upward
saccades after VPIN inactivation were significantly larger than
saccades to the same target before inactivation, increasing from
~10° to as large as ~17° (Fig. 3D, monkey
2, up). Normally 17° saccades exhibit a higher peak velocity
than 10° saccades (Fuchs 1967). Yet after bilateral
VPIN inactivation, hypermetric upward saccades reached peak velocities
that were the same as or lower than those of normal saccades (Fig. 6).
Thus it seems that saccades made after VPIN inactivation do not conform to the normal relation between saccade size and peak velocity, called
the "main sequence" (Bahill et al. 1975
).
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Saccade latency
Neither uni- nor bilateral inactivation of the VPIN caused a consistent change in the latency of saccades to 10° target displacements. For example, unilateral VPIN inactivation increased the latency of most types of horizontal saccades in monkey 1 (not leftward centripetal) by 10-20 ms but either decreased or did not affect the latencies of horizontal saccades in monkeys 2 and 3. Unilateral inactivation decreased (monkey 1), increased (monkey 2), or did not affect (monkey 3) the latencies of upward centrifugal saccades and did not significantly change the latency of upward centripetal saccades in any monkey. Downward saccades showed similarly mixed effects after unilateral inactivation. Bilateral inactivation did not significantly change the latency of any type of saccade except for increasing the latency of downward saccades in monkey 2 by ~40 ms.
Postsaccadic drift
After bilateral VPIN inactivation in monkey 2, a slow upward drift often followed upward saccades. No drift followed downward saccades. In monkey 3, upward saccades before inactivation were often followed by a downward drift. After bilateral VPIN inactivation this drift was rarely evident. Again, no drift followed downward saccades.
To characterize this drift, I measured eye velocity in the first 50 ms following 14-77 vertical saccades in both monkeys. Figure 8 shows average eye position records and the average velocity of the drift following vertical saccades in each monkey. In monkey 2 bilateral VPIN inactivation caused a significant increase in the average velocity of upward drift after upward saccades, from 1.87 to 5.42°/s. It also caused a significant, but very small, change in the average velocity of drift after downward saccades, i.e., from downward 0.4 to upward 0.79°/s. In monkey 3, which normally had a large downward drift of 10.52°/s after upward saccades, bilateral VPIN inactivation significantly reduced drift velocity to 2.75°/s and caused no significant change in the drift following downward saccades, i.e., from downward 1.25 to 0.04°/s. Thus in both monkeys, bilateral VPIN inactivation added a significant upward velocity to the drift following upward but not downward saccades.
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Nonoculomotor deficits
None of the monkeys showed severe postural instability on return to their home cages after inactivation of one or both VPINs. However, they all seemed to have difficulty moving their arms accurately to retrieve food offered by hand or from the hopper attached to their cages. A typical example occurred when monkey 2, with both VPINs inactivated, tried to reach into a circular hole (~50 mm diam) in the food hopper in the front of its cage. The first reach missed to the left of the hole. The monkey withdrew its arm and tried again, this time missing to the right. The next reach again missed to the left. After five misses to alternating sides of the hole the monkey changed strategy and pushed its hand gently against the front surface of the hopper to one side of the hole. It then moved its hand along the surface of the hopper toward the hole until its hand went through the hole and retrieved a biscuit. It had no trouble grasping the biscuit. Ordinarily this monkey never missed while reaching through the hole nor did it use the alternate strategy at any other time.
The monkeys showed no evidence of dizziness, disorientation, or nausea after any of the injections. During testing they tracked the spot for the same amount of time that they did when their VPINs were not inactivated and were calm and eager eat. In their home cages after injections they were calm and ate food offered to them.
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DISCUSSION |
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The major finding of this study is that inactivating the VPIN with muscimol made upward saccades too large and downward saccades too small. Generally these dysmetrias reflected changes in saccade gain rather than offset. In two of the three monkeys, VPIN inactivation also caused horizontal saccades to angle upward so that they ended above their targets.
Our muscimol injections almost certainly affected saccades by
inactivating saccade-related neurons in the VPIN. I recorded saccade-related activity at each injection site immediately before each
injection. Marking lesions confirm that the activity recorded was in
the VPIN. The reaching deficit evident after the VPIN inactivation probably resulted from spread of muscimol to adjacent limb-related areas of the posterior interpositus nucleus. This deficit is similar to
that of monkeys receiving muscimol injections into the limb-related part of the posterior interpositus nucleus. Such injections cause deficits in directing the ipsilateral arm accurately but not in using
the hands to grasp (Mason et al. 1998).
Role of the VPIN in saccades
VPIN inactivation caused saccades in all directions to end above their targets (with the exception of horizontal saccades in monkey 3). A simple explanation for this effect is that VPIN activity drives the eyes downward. This, however, does not explain why bilateral inactivation made downward saccades decelerate slower than normal and sometimes made upward saccades accelerate slower than normal and reach lower than normal velocities (Fig. 6, C and D, Table 2, Fig. 7). To account for these effects, I propose that some VPIN neurons add an upward drive to saccades while others add a downward drive. Inactivating all VPIN neurons deprives saccades of both upward and downward drive so that both upward and downward saccades accelerate and decelerate slower than normal and reach slower than normal peak velocities. If this proposal is correct, the downward drive must outweigh the upward drive to account for postinactivation saccades ending above their targets.
If downward and upward drives were nearly equal, bilateral VPIN inactivation would cause only small changes in saccade gain and direction but would still reduce saccade acceleration, deceleration, and peak velocity. This is the pattern monkey 3 exhibited. Bilateral VPIN inactivation may have affected monkeys 2 and 3 differently because upward and downward drives from monkey 3's VPINs were more nearly balanced.
How does the VPIN influence saccades?
The VPIN projects to two structures that could influence the
vertical component of saccades, the superior colliculus and the INC.
Axons from the VPIN and the adjacent dentate nucleus terminate throughout a large part of the intermediate layers of the contralateral superior colliculus (May et al. 1990), an area
representing saccades of many sizes and directions, including,
presumably, vertical saccades. There is currently no information about
the VPIN influence on the superior colliculus.
The VPIN also sends a projection to the contralateral INC, though this
projection is described is "sparse" (May et al.
1992). The description of this projection comes from a large
stereotaxically placed injection of tracer into the posterior
interpositus nucleus. There is no indication that this injection
included many saccade-related VPIN neurons, and so it may not
accurately show how large the projection is from the VPIN to the INC.
The VPIN projection to the INC could influence the vertical component
of saccades. The INC contains many saccade-related burst and
burst-tonic neurons with vertical on directions (Dalezios et al.
1998; Helmchen et al. 1996
), and INC axons
terminate in the trochlear nucleus and in the parts of the oculomotor
nucleus related to vertical movements (Horn and
Büttner-Ennever 1998
; Kokkoroyannis et al.
1996
; Steiger and Büttner-Ennever 1979
). As its efferent connection lead us to expect, lesions of the INC in cat
(Fukushima and Fukushima 1992
) and monkey
(Helmchen et al. 1998
) severely impair vertical saccades.
Postsaccadic drift
Why does bilateral VPIN inactivation add upward velocity to the eye immediately after upward but not downward saccades? Many VPIN neurons exhibit a burst for upward saccades that continues as much as 50 ms beyond saccade end. Bursts for downward saccades often end before or near saccade end (F. R. Robinson, A. F. Fuchs, and A. Straube, unpublished observations). If the activity of these neurons drives the eyes downward, the extended burst for upward saccades would apply a downward drive to the eyes for ~50 ms after saccade end. Removal of VPIN activity with muscimol would remove this postsaccadic downward drive, effectively adding an upward component to eye movement after the saccade. This explanation is consistent with VPIN activity but does not explain why it is necessary for the VPIN to normally provide a downward drive to the oculomotor system after upward, but not downward, saccades.
Differences between the VPIN and CFN
Some VPIN neurons increase their firing rate with decreasing
vergence angle and accommodation and thus are called "far response neurons" (Zhang and Gamlin 1998). These cells are in
the same area as neurons with saccade-related responses, but no neuron exhibits sensitivity to both the vergence and saccades. In contrast, CFN neurons increase their firing rate during increases in vergence angle and accommodation, i.e., the near response (Zhang and
Gamlin 1996
). CFN inactivation with muscimol reduces vergence
speed and size (Gamlin and Zhang 1996
). Sixty-three
percent of CFN neurons that respond to convergence also modulate during
saccades (Zhang and Gamlin 1996
).
A role of the CFN in convergence may be consistent with the proposal
that CFN activity on one side drives the eyes toward the contralateral
side. CFN activity could aid convergence by driving the ipsilateral eye
nasally. This could happen only if the activity of some CFN neurons
influenced movements of the ipsilateral eye more than movements of the
contralateral eye. CFN neurons have not been tested for unequal
influence on the movements of the two eyes, but it is possible that
they have such influence because other neurons show it. Unequal
influence on the two eyes has been described in preoculomotor neurons
in the brain stem (Zhou and King 1998) and in
unidentified neurons in the cerebellar nuclei (Zhou and King
1996
). If, as VPIN inactivation indicates, VPIN activity
influences the vertical component of saccades, this activity is
unlikely to affect the relative angle of the eyes. There may be no VPIN
neurons sensitive to both vergence and saccades because there would be
no functional advantage to saccade-related VPIN activity during vergence.
Although CFN clearly influences the vertical component of saccades, its
strongest influence is on the horizontal component (Robinson et
al. 1993). VPIN seems concerned almost entirely with the
vertical component. This is the best answer we currently have to why
neurons in both the CFN and VPIN burst during nearly every saccade,
i.e., each area contributes distinct components of every saccade.
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ACKNOWLEDGMENTS |
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I gratefully acknowledge C. Noto, S. Usher, and D. Reiner for help with surgery, animal training, and data collection. I am also grateful to A. Fuchs for reading an earlier draft of this paper, to B. Cent for writing and maintaining the software for saccade analysis, and to K. Elias for editing the manuscript. Thanks to B. Brown and the veterinary care staff at the Regional Primate Research Center for the excellent care of the animals.
This study was supported by National Institutes of Health Grants RR-00166 and EY-10578.
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FOOTNOTES |
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Address for reprint requests: Dept. of Biological Structure, Box 357420, University of Washington, Seattle, WA 98195-7420 (E-mail: robinsn{at}u.washington.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 3 May 1999; accepted in final form 11 May 2000.
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REFERENCES |
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