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The Journal of Neurophysiology Vol. 79 No. 3 March 1998, pp. 1286-1294
Copyright ©1998 by the American Physiological Society
Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140
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ABSTRACT |
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 Abstract
 Introduction
Methods
Results
Discussion
References
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McElligott, J. G., Phyllis Beeton, and Jeffrey Polk. Effect of cerebellar inactivation by lidocaine microdialysis on the vestibuloocular reflex in goldfish. J. Neurophysiol. 79: 1286-1294, 1998. Vestibuloocular reflex performance and adaptation were examined during vestibulocerebellar inactivation by localized lidocaine microdialysis or injection in goldfish. In the light, eye velocity perfectly compensated for head velocity (Vis-VOR) during sinusoidal yaw rotation (1/8 Hz ± 20°). In the dark, the reflex (VOR) gain was slightly reduced (gain 
0.8-0.9). In neither Vis-VOR nor VOR, was gain altered after 1 h of lidocaine microdialysis in the vestibulocerebellum. Before adaptation of reflex gain, the initial suppression or augmentation of Vis-VOR reflex gain produced by in-phase or out-of-phase visual-vestibular stimulation was also unaffected by cerebellar inactivation. Subsequently, 3 h of adaptive reflex training in either the in-phase or out-of-phase paradigm (acquisition phase) respectively decreased (0.30 ± 0.09) or increased (1.60 ± 0.08) VOR gain during artificial cerebral spinal fluid (CSF) microdialysis. However, microdialysis of lidocaine completely blocked adaptive gain changes during a 3-4 h period of continuous application. This effect was reversible because VOR gain changes were produced 1 h after lidocaine was replaced with CSF as the dialysate. After adaptive training, bilateral CSF injections (0.25 µl/side) into the vestibulocerebellum did not alter the normal retention or decay of adapted gain changes during a 3 h period in the dark (retention phase). However, injection of lidocaine into the vestibulocerebellum completely blocked retention of the adapted VOR gain returning the gain to values recorded before adaptation. In contrast to either acute or chronic surgical removal, lidocaine inactivation of the cerebellum by microdialysis did not alter either Vis-VOR and VOR behavior or interactive Vis-VOR performance over a wide range of gain extending from 0.3 to 1.4. Thus short-term VOR motor learning is a dynamic process requiring either continuous operation of brain stem cerebellar loops or, alternatively, modifiable sites within or directly influenced by the cerebellum. Our data supports the latter hypothesis, because the direct brain stem VOR pathways appear to be unaltered after cerebellar inactivation, and, hence, independent of the VOR-adapted state.
The vestibuloocular reflex acts to minimize slippage of an image on the retina in the presence of head movements. This reflex has served as an exceptional model to study sensorimotor integration in the central nervous system (CNS). Adaptation of the reflex has also provided us with a model system for the investigation of information acquisition, storage, and retrieval involving neuroplastic changes in the CNS (see du Lac et al. 1995 Subjects and initial setup procedures
Goldfish (length, 10-15 cm; nose tip to peduncle) acquired from Huntington Creek Fisheries (Thurmont, MD) were housed in laboratory aquaria (20- or 30-gallon tanks) at 20°C. All animals, maintained on a 12-h light:dark cycle, were acclimated to these tanks for at least 2 weeks before testing.
Experimental equipment and behavioral procedures
VESTIBULAR AND VISUAL APPARATUS.
The vestibular table, driven by a position and velocity feedback servo-controlled motor (Inland Motor, Radford, VA) was located in a separate light-proof room. The electromagnetic field generating coils and cylindrical test aquarium were mounted on this table. A planetarium (Biomedical Engineering, Thornwood, NY) controlled by a second servomotor was placed directly above the fish's head. This displayed a random dot stimulus pattern of light on the inside surface of the cylindrical test aquarium. Goldfish follow whole field visual targets for extended periods with no diminution of the response during visuovestibular stimulation.
BEHAVIORAL PROTOCOLS.
The terms visual vestibuloocular reflex (Vis-VOR) and vestibuloocular reflex (VOR) are used in this study to depict the operation of this reflex, respectively, in the light and dark during vestibular stimulation before adaptation. Vis-VOR gain equal to one was produced when the visual stimuli of the planetarium were held in an earth fixed position during sinusoidal table rotation (1/8 Hz at ± 20°; maximum velocity = 15.7°/s). Gain of the reflex is defined as the ratio of eye to head velocity. In-phase sinusoidal rotation of the table and planetarium together suppressed Vis-VOR gain. Augmented Vis-VOR gain was produced by presentation of the visual and vestibular stimuli 180° out of phase but with the amplitude of planetarium rotation twice that of the vestibular table, i.e., 1/8 Hz at ± 40° (maximum velocity = 31.4°/s). This is a Vis-VOR gain condition equal to three. It produces the same initial augmentation as a gain condition equal to two (table and planetarium sinusoidally rotated at the same amplitude but 180° out of phase). However, fish adaptively trained to increase gain towards three produce larger gain increases than those trained towards a gain of two, thus allowing for a clearer evaluation of adapted reflex gain. Fish are capable of following the stimuli at a gain of three (maximum stimuli velocity = 47.1°/s). Past experimentation has shown that there is a linear relation between head and eye velocity over a wide velocity range up to 64°/s (Pastor et al. 1992 EYE MOVEMENT MEASUREMENT.
Calibration was performed with a test search coil mounted in the tank. At the beginning of each experiment, calibrations for each fish were carried out before and after modification of the Vis-VOR and the VOR. Gain of the reflex was determined in the light at the following gain conditions: 1) set equal to one (Vis-VOR), 2) set to increase gain toward three (Vis-VOR augmentation), 3) set to decrease gain toward zero (Vis-VOR suppression), and 4) in the dark (VOR). After these initial measurements of the reflex gain, adapted gain increases and decreases were produced over a 3-h period. During the experiments, position and velocity signals from the vestibular test table, planetarium, and both eyes were recorded. During adaptation, reflex gain measurements in the light and dark were made every 15 min during the first hour and every 30 min during the second and third hour of the acquisition phase. During the retention phase of adpatation (duration = 3 h), goldfish were held stationary in the dark and only rotated for two 50-s periods for each time point when the VOR recordings were made after the same schedule as during the acquisition phase.
Data analysis
SINUSOIDAL STIMULATION.
For determination of reflex gain, head (vestibular table), planetarium, right and left horizontal eye position signals were individually amplified and recorded. Each of the signals was collected by computer at 50 samples/s per channel during a 50-s test period. Fast phases (saccades and eye blinks) were removed and signals were reconstructed from the remaining slow-phase eye movements. Gain was determined by a comparison of the Fast Fourier Transform (FFT) of head (vestibular table) and reconstructed eye signals. Gain was defined as the ratio of the coefficients at the fundamental frequency (1/8 Hz) of table and head rotation. For each condition tested, gain was determined by averaging two separate data samples of 50 s each. To obtain an estimate of the effect of lidocaine on the VOR for both eyes, the individual gains for the right and the left eye were averaged together to obtain a single measure of reflex gain to compensate for any bias that could have been introduced by the infusion laterality. The analysis procedure was similar to the method used in our previous studies of VOR adaptation (Li et al. 1995 Microinjection and microdialysis procedures
After initial vestibuloocular reflex calibrations, lidocaine (4% lidocaine hydrochloride, Roxane Lab, Columbus, OH) or a control agent [artificial fresh-water fish cerebral spinal fluid (CSF)(in mM): 100.00 NaCl, 2.49 KCl, 1.00 MgCl6·H2O, 0.44NaH2PO4·H2O, 1.13 CaCl2·2H2O, and 5.00 NaHCO3; final pH = 7.2] was infused into the vestibulocerebellum via a microdialysis or bilateral microinjection probe inserted ~2 mm into the caudal-dorsal surface of the vestibulocerebellum centered with respect to the midsagittal plane (Fig. 1).
STATISTICAL ANALYSES.
Analysis of variance for repeated samples were used initially to determine the significance (P This study investigated the effect of cerebellar inactivation on the performance and adaptation of the vestibuloocular reflex by discrete application of lidocaine into the vestibulocerebellum before, during, and after training goldfish to produce adaptive gain increases or decreases.
Effects of lidocaine within the vestibulocerebellum on the Vis-VOR and VOR
Before adaptation and lidocaine application, goldfish were sinusoidally rotated about the vertical axis within a stationary visual field (1/8 Hz at ±20°). Typical slow-phase eye movements of a fish in this condition have unity gain (Fig. 2, Initial, Vis-VOR; gain = 1.02). Recordings taken when the visual stimulus was sinusoidally rotated at the same frequency, but 180° out of phase or in phase with the fish, respectively, augmented or suppressed Vis-VOR reflex gain (Fig. 2, Initial; augmentation gain = 1.31; suppression gain = 0.15). The VOR reflex gain in the dark was equal to 0.88 for this animal. For each stimulus condition presented in Fig. 2, Initial, the two tracings depict raw eye position signal (top), including fast and slow phases and the reconstructed slow phase movements (bottom) after fast-phase removal.
Effects of lidocaine on the acquisition phase of Vis-VOR and VOR adaptation
Eye movements of individual goldfish that underwent adaptive vestibuloocular reflex training to increase VOR gain while lidocaine or CSF was dialyzed into the vestibulocerebellum are presented in Fig. 3A. Before adaptive training to increase VOR gain, one fish was dialyzed with lidocaine and a second fish with CSF for 1 h before the beginning of gain increase adaptation. The eye movements displayed in Fig. 3A show that similar VOR gains were recorded in both cases before adaptive training (Lidocaine, gain = 0.89; CSF, gain = 1.00). However, after 3 h of training, the VOR gain of the CSF animal increased to 1.96, whereas the gain of the lidocaine animal remained essentially unchanged at 0.99. Another goldfish, trained to decrease VOR gain during lidocaine microdialysis, had similar gains before (0.80) and after (0.90) adaptation (Fig. 3B). However, a goldfish dialyzed with CSF readily decreased gain from 0.83 to 0.20 during the 3-h adaptation period.
Effects of lidocaine on the retention phase of Vis-VOR and VOR adaptation
A second set of experiments was carried out to test the effect of cerebellar inactivation by lidocaine on retention of a previously adapted VOR gain decrease or increase. Four lidocaine and five CSF injected fish were employed in those experiments involving gain decreases (Fig. 5A). A bilateral tapered injection probe was used instead of the microdialysis probe to observe the immediate effect of a single intracerebellar lidocaine injection. Probe insertion did not alter Vis-VOR (data not shown) or the VOR gain (Before vs. After Probe Insertion; Acquisition at t = 0 h Fig. 5A; NS, t-test). The probe was inserted before the acquisition period to minimize disturbance to the animals' reflex between the acquisition and the retention phases of adaptation. During the 3 h acquisition phase, VOR gain decreased in a similar manner for both groups of animals. Bilateral injection of 0.25 µl/side CSF or lidocaine was carried out over a 5-min period at the end of the acquisition phase (Fig. 5A). Fifteen minutes later, VOR gain measurements at the beginning of the retention period were made (Retention at 0 h).
Recovery of adaptation after cerebellar lidocaine microdialysis
Lidocaine is a local anesthetic agent whose duration is short (~1 h). Therefore after diffusion and metabolism of the drug, cerebellar function should be restored. To determine that the inhibition of VOR adaptation was due to a temporary anesthetic effect and not to tissue or other permanent destruction, an additional series of experiments was conducted. As in the previous experiment, lidocaine was dialyzed into the cerebellum for 1 h before adaptive training. Thereafter, lidocaine microdialysis continued during 3 h of training either to increase (n = 2), or to decrease (n = 2) VOR gain. Comparison of the respective gains at t =
VOR and Vis-VOR gain is unchanged by cerebellar inactivation
Previous studies have shown that the surgical removal of the cerebellum results in a change in VOR gain (Godaux and Vanderkelen 1984 Acquisition and retention of adapted VOR and Vis-VOR gain
Previous studies (see INTRODUCTION) showed that permanent chemical or surgical cerebellectomy in a variety of mammalian species eliminates adaptation of the vestibuloocular reflex irreversibly. Usually, these studies assay adaptation several days after removal of the cerebellum's influence on the brain stem circuitry. However, one study (Luebke and Robinson 1994
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
for review). This reflex has been characterized as operating via a three neuron pathway involving the semicircular canals, the vestibular and oculomotor nuclei, and the extraocular muscles (Szentágothai 1950). The cerebellum, or more specifically the vestibulocerebellum, also plays a prominent role in the reflex. There has been a consensus supporting the view that the Purkinje cells modulate the gain of the vestibuloocular reflex via inhibitory input to vestibular neurons (Ito 1972; Lisberger and Sejnowski 1992; Miles and Lisberger 1981; Robinson 1981).
and Albus (1971) and the specific formalization by Ito (1972) directly implicated the cerebellum in vestibuloocular reflex adaptation. Experimentation in mammals have shown that removal of the vestibulocerebellum by chemical or surgical lesions can alter the gain of the vestibuloocular reflex. For example, different studies have reported that postlesion reflex gain is elevated in cats (Robinson 1976); depressed in cats (Godaux and Vanderkelen 1984; Keller and Precht 1979; Precht and Anderson 1979; Torte et al. 1994), monkey (Lisberger et al. 1984), and rabbit (Ito et al. 1974b, 1982); or unchanged in monkey (Zee et al. 1981). Moreover, adaptation of the vestibuloocular reflex, manifested as changes in reflex gain, was eliminated. In addition, subsequent postlesion attempts to adapt reflex gain failed.
; Pastor et al. 1994b) showed that immediately after cerebellectomy there is an increase in VOR gain and also that retention of a previously adapted gain change is eliminated. Pastor et al (1994b) also reported that adapted changes in the earliest (<50-70 ms) part of the reflex were maintained and partial recovery of adaptive capability occurs 2-3 months after cerebellectomy.
). Stimulation of the inferior olive at 7 Hz produced climbing fiber activation that in turn prevented the transmission of simple spike activity in 95% of the floccular Purkinje cells recorded. Because longer-term (3 days) adapted vestibuloocular reflex gain increases or decreases were preserved under this condition, it was concluded that the modifiable synapses responsible for vestibuloocular reflex adaptation are located not in the cerebellum but at an extracerebellar site in the brain stem. The results of this report are in conflict with the previously cited investigations, which demonstrated that adapted VOR gain changes are eliminated after cerebellectomy.
METHODS
Abstract
Introduction
Methods
Results
Discussion
References
).
; McElligott et al. 1995).
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FIG. 1.
Sagittal section of a goldfish brain illustrating location of a microdialysis probe in vestibulocerebellum. Only dialysis membrane (176 µm diam, 2 mm length) of probe was inserted into cerebellum. From caudal to rostral, structures identified are, vagal lobe (VL), cerebellum (CB), and valula cerebelli (VC). Within goldfish cerebellum, dark area penetrated by schematically represented dialysis probe is granular cell layer. Vestibulocerebellum is located just dorsal to tip of microdialysis probe. Other illustrative figures locating vestibulocerebellum in goldfish can be found in Pastor et al (1994a ,b). Goldfish cerebellum in these other papers has a more erectile profile because of tissue fixation. Cerebellum shown above is from frozen unfixed tissue. Scale bar = 1 mm.
). After the first calibration of vestibuloocular reflex, the dialysis probe was inserted and lidocaine or artificial CSF was delivered, commencing 1 h before the initiation of reflex adaptation. During this period goldfish were sinusoidally rotated in the gain equals one condition. A final set of calibrations was then taken just before the beginning of adaptation.
0.01) or nonsignificance (NS) of the data by using StatView (Version 4.02; Abacus Concepts, Berkeley, CA). If statistically significant differences were found, then multiple t-test comparisons were performed. When average gains are reported in the paper, they are reported as the means ± SE.
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
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FIG. 2.
Visual vestibuloocular reflex (Vis-VOR) and vestibuloocular reflex (VOR) recordings before and after cerebellar lidocaine microdialysis before experimental vestibuloocular reflex gain adaptation. Each panel in this figure shows raw (slow and fast phase, top) and reconstructed (slow phase, bottom) eye movements. Initial: this illustrates Vis-VOR (gain condition set equal to 1), augmented Vis-VOR, suppressed Vis-VOR, and VOR recorded before cerebellar lidocaine infusion. Lidocaine Microdialysis: these recordings were taken after 1 h of lidocaine microdialysis in vestibulocerebellum. During period of microdialysis, animals were rotated in Vis-VOR gain condition = 1. Cerebellar inactivation by lidocaine microdialysis did not alter Vis-VOR or VOR gain during any of stimulus conditions. Number included with each data set represents reflex gain of reconstructed eye movements as determined by Fast Fourier Transformation (FFT) analysis.
).
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TABLE 1.
Vestibuloocular reflex gain before and after vestibulocerebellar microdialysis
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FIG. 3.
Lidocaine but not cerebral spinal fluid (CSF) microdialysis into vestibulocerebellum prevents adaptive VOR gain changes. A: eye movement recordings show that VOR gains of a fish microdialyzed with lidocaine were similar before (Before Adaptive Training) and after (After Adaptive Training) 3 h of training to increase gain. In contrast, adapted-VOR gain increases were recorded in another goldfish during CSF microdialysis. B: data presented respectively from 2 other goldfish show that adaptation to decrease gain is also prevented by lidocaine but not CSF microdialysis. Raw (top) and reconstructed (bottom) eye movements as well as calculated gains are presented for each data panel.
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FIG. 4.
Effects of lidocaine and CSF infusions on adapted gain control. A: eye-movement data for Vis-VOR (open symbols) and VOR (solid symbols) in goldfish trained to increase (n = 9; 
, 
) or decrease (n = 4; 
, 
) gain over a 3-h period during lidocaine microdialysis into vestibulocerebellum. B: eye movement data from goldfish trained to increase (n = 5) or decrease (n = 3) gain during CSF microdialysis. Only CSF-microdialyzed goldfish produced statistically significant (* P 0.01; 1-way analysis of variance) VOR gain changes. Data presented are means ± SE.
64 %) or increase (+113%) after 3 h of adaptation (P < 0.01; 1-way ANOVA). A significant change in the Vis-VOR gain was also evident for the gain increase animals (from 1.36 ± 0.03 to 2.67 ± 0.26; Fig. 4B). For the gain decrease animals, only a small but nonsignificant change in the Vis-VOR was noted because these animals are capable of suppressing the Vis-VOR reflex at the beginning of adaptation (from 0.33 ± 0.06 to 0.22 ± 0.06; NS; 1-way ANOVA).
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FIG. 5.
Effects of lidocaine and CSF infusions on retention of adapted gain. A: 2 groups of goldfish were trained to decrease VOR gain after bilateral microinjection probes were placed in vestibulocerebellum. After 3 h of adaptive training (Acquisition), they were injected bilaterally (0.25 µl/side) with lidocaine ( 
) or CSF (
). Lidocaine injected goldfish (n = 4) immediately lost adapted VOR gain decrease component. Adapted gain decrease gradually returned over a 3 h retention period (Retention) after diffusion and metabolism of lidocaine. CSF injected animals maintained adapted VOR gain decrease throughout retention period. B: a similar experiment was carried out for animals trained to increase VOR gain. Lidocaine injection also resulted in immediate loss of adapted VOR gain increase. No return of adapted gain increase was observed because CSF-injected animals normally lose their adapted gain increase over 3-h retention period. Fifteen minutes (broken line) intervened between end of adaptation period and beginning of retention period when microinjection took place. Data are presented as means ± SE.
).
0.01, t-test). Again, the VOR gain after lidocaine injection was equal to that recorded before adaptation (Acquisition at 0 h; gain = 0.95 ± 0.06). During the retention phase, there was no significant change in the magnitude of the VOR gain (Retention at 3 h; gain = 1.00 ± 0.18). For the CSF-injected animals, there was a small but nonsignificant loss of adapted VOR gain change (from1.83 ± 0.20 to 1.51 ± 0.24; NS; t-test). Inspection of the retention part of the curve in Fig. 5B, illustrates that over the 3-h period there is a gradual loss of adaptation in the CSF injected animals. In other studies, we have observed a similar loss of retention for adapted gain increases in intact animals that had not received any cerebellar injection. Thus this loss over 3 h appears normal and cannot be attributed to the injection itself. Holding goldfish in the dark during retention contributes to this loss of adaptation as has been shown in other studies from our lab (McElligott 1997).
1 h and t = 0 h presented in Fig. 6 illustrates that probe insertion and lidocaine microdialysis for 1 h did not alter reflex gain when goldfish were stimulated to decrease or increase Vis-VOR gain or when tested in the dark (VOR).
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FIG. 6.
Reversal of adapted gain control cancellation. Gains for Vis-VOR ( , ) and VOR (, ) gains of goldfish trained to increase (n = 2; , ) or decrease (n = 2; , ) reflex gain during lidocaine (4 h) and then CSF (5 h) microdialysis into vestibulocerebellum. Adaptive training to alter VOR gain began after 1 h of lidocaine microdialysis (at t = 0 h). Gain decreases or increases were detected 1 h after (at t > 4 h) initiation of CSF microdialysis. Data presented are means ± SE.
increase gain = +1.05, from 0.93 ± 0.16 to 1.98 ± 0.06 and decrease gain = 0.51, from 0.87 ± 0.19 to 0.36 ± 0.02, respectively). These adaptive changes were comparable to that produced in the control CSF dialyzed fish (Fig. 4B) in the earlier experiments. Similar adaptive gain changes were evident in the Vis-VOR for animals trained to increase gain but not for the animals trained to decrease gain ( increase gain = +1.05, from 1.50 ± 0.10 to 2.55 ± 0.13 and decrease gain = 0.10, from 0.28 ± 0.14 to 0.18 ± 0.04, respectively). Goldfish produce only small adaptive Vis-VOR gain decreases because they are capable of suppressing their Vis-VOR gain before adaptation. Thus the effect of lidocaine on VOR adaptation when infused into the vestibulocerebellum was reversed.
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
; Ito et al. 1974b, 1982; Keller and Precht 1979; Lisberger et al. 1984; Nagao 1983; Precht and Anderson 1979; Robinson 1976; Torte et al. 1994). Because measurements in these mammalian studies were made several days after cerebellectomy, some neuronal reorganization could account for the gain change. However, this cannot be the sole factor because goldfish (Michnovicz and Bennett 1987; Pastor et al. 1994b) also produced gain changes when measurements were made immediately after cerebellectomy. All these results contrast with our findings reporting no alteration in VOR gain after cerebellar lidocaine inactivation. It is important to point out that lidocaine microdialysis reversibly inactivates only the neurons localized in the vestibulocerebellum, whereas cerebellectomy traumatically removes the entire structure.
) or chemical (Ito et al. 1982) flocculectomy results in a loss of the ability to suppress the Vis-VOR on the side of the lesion. Similar results have been reported for cats (Torte et al. 1994) and monkeys (Zee et al. 1981) after flocculectomy. Decreases in optokinetic gain after floccular lesions have also been shown to occur in rabbit (Ito et al. 1982; Nagao 1983), cat (Torte et al. 1994), and monkey (Takemori and Cohen 1974). However, past findings are not entirely in agreement because there are also reports of no loss in Vis-VOR gain suppression in both goldfish (Michnovicz and Bennett 1987; Schairer and Bennett 1981) and cats (Keller and Precht 1979) after cerebellectomy.
; Korp et al. 1989; McCrea and Baker 1985). In goldfish, Pastor et al (1994a) proposed that Area II, a brain stem nucleus, serves a role similar to the hypoglossus nucleus. This latter study also demonstrated that lidocaine inactivation of Area II, reduces the gain of both the optokinetic and vestibuloocular reflex. In our study it appears that the brain stem pathways are sufficient to maintain the normal performance and modulation of the Vis-VOR. Past studies in goldfish (Allum et al. 1976), cat (Keller and Precht 1979), and monkey (Waespe and Cohen 1983; Zhang et al. 1995) have shown that optokinetic and vestibular derived neural activity are recorded from the same neurons in the vestibular nucleus during multisensory stimulation. However, without the influence of the cerebellum they do not support the production of short-term adaptive gain changes.
; Keller and Precht 1979) noted that vestibular nuclei are more than simple relay centers and act by integrating vestibular and visual information. This provides goldfish with adequate information to maintain normal performance levels for the vestibuloocular reflex.
) used a reversible electrophysiological procedure termed floccular shutdown. During this experiment, Luebke and Robinson stimulated the inferior olive unilaterally at 7 Hz activating the climbing fiber system and thereby silencing simple spike firing in 95% of the floccular Purkinje cells. In this study, these investigators reported that "deadaptation" (i.e., return from adapted to preadapted gain levels), as well as retention of a longer-term VOR gain change (after 3 days of adaptation) was not altered by floccular shutdown. Thus these investigators concluded that the site of VOR adaptation does not reside within the cerebellum.
; Raymond et al. 1996). In addition, the experiments of Luebke and Robinson involved deadaptation and not adaptation per se.
; Robinson 1976) have shown that cats readily produce significant short-term adaptive changes. Equally important would be an experiment that uses lidocaine inactivation on longer term (days) adaptive VOR gain changes.
, our results agree with the previous work in mammals showing that removal of the cerebellum chronically prevents acquisition and inhibits retention of adapted gain increases and decreases. In goldfish studies (Michnovicz and Bennett 1987; Pastor et al. 1994b) a loss in retention of an adapted VOR gain change also occurred immediately after removal of the cerebellum. Thus this alteration in the gain must be due to the cerebellectomy and not due to the subsequent neuronal reorganization that could have occurred in the mammalian studies when measurements made several days later.
. In this latter study, both the dynamic (early) and sustained (late) VOR components were measured by using a velocity step stimulus. Our results with sinusoidal stimuli can only be compared with the sustained results of Pastor et al (1994b). In addition, their study assayed the effect of cerebellectomy for a period of >6 mo. These authors reported that there is a partial restoration of VOR adaptive capability 2-3 mo after cerebellectomy. Our work demonstrated that short-term (hours) acquisition and retention of adaptive capability is completely but reversibly lost after lidocaine inactivation of the vestibulocerebellum.
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ACKNOWLEDGEMENTS |
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We thank the reviewers for constructive criticisms in evaluating this manuscript.
This work was supported by a National Institute of Deafness and Communicative Disorders Grant R01 DC-01094.
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FOOTNOTES |
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Address reprint requests to J. G. McElligott.
Received 11 January 1997; accepted in final form 28 November 1997 .
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REFERENCES |
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Abstract
Introduction
Methods
Results
Discussion
References
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