Biomedical subjects

E Godaux

Publications and source records attributed to E Godaux.

At least 55 records · Page 3Linked to original sources

PubMed1995

Neuronal activity in the ipsilateral vestibular nucleus following unilateral labyrinthectomy in the alert guinea pig.

1. Neuronal activity was investigated in the left superior vestibular nucleus (SVN), lateral vestibular nucleus (LVN), and rostral part of the medial vestibular nucleus (MVN) in the alert guinea pig after a unilateral (left) labyrinthectomy was performed. Vestibular neurons were recorded either immediately (just-postoperative group, n = 6) or 1 wk after labyrinthectomy (1-wk-postoperative group, n = 6) and compared with the activity recorded in intact animals (control group, n = 6). 2. Animals were prepared for extracellular recording of single-unit activity and for eye movement recording (scleral search coil technique). To enable stimulation of the left vestibular nerve, bipolar silver ball electrodes were chronically implanted either in contact with the bony labyrinth in the control group or close to the stump of the vestibular nerve after labyrinthectomy. Complete labyrinthectomy was performed under halothane anesthesia. 3. The criterion used to select vestibular neurons for analysis was their recruitment by an electric shock on the vestibular nerve. Of the 589 recorded neurons, 424, defined as second-order vestibular neurons, were recruited at monosynaptic latencies (0.85-1.15 ms) and 165 were recruited at polysynaptic latencies. One hundred three second-order vestibular neurons were recorded in the control group, 173 in the just-postoperative group, and 148 in the 1-wk-postoperative group. 4. The activity of the electrically recruited neurons was recorded during sinusoidal horizontal head rotation in the dark (0.3 Hz, 40 degrees/s peak velocity). The behavior of the neurons was analyzed by plotting their firing rate against head velocity. The Y-intercept of the regression line was used to express spontaneous firing rate (resting discharge), and its slope was used to express the sensitivity of the neuron-to-head velocity. 5. In the absence of statistically significant difference between the characteristics of the neuronal discharge of the second-order vestibular neurons recorded in the SVN, LVN, and rostral MVN, the data were pooled. The Resting discharge of these cells amounted to 41.0 +/- 24.7 (SD) spikes/s in the control state, fell to 7.2 +/- 13.9 spikes/s just after labyrinthectomy, and completely returned to normal values 1 wk after surgery (42.5 +/- 21.6 spikes/s). Among the monosynaptically recruited neurons, the percentage of silent units was 0% in the control group, 69% in the just-postoperative group, and 0% in the 1-wk-postoperative group. 6. By contrast, the sensitivity to head velocity of the second-order vestibular neurons, which was 0.69 +/- 0.48 (SD) spikes.s-1/deg.s-1 in the control state and which fell to 0.03 +/- 0.11 spikes.s-1/deg.s-1 just after labyrinthectomy, remained low 1 wk after injury (0.21 +/- 0.26 spikes.s-1/deg.s-1). Moreover, the slight recovery of sensitivity to head rotation was due only to units behaving as type II neurons. 7. The mean resting discharge of the polysynaptically recruited neurons (pooled from the 3 explored nuclei) was 31.6 +/- 19.3 spikes/s in the control group. It decreased to 11.6 +/- 12.1 spikes/s in the just-postoperative group and recovered to 39.8 +/- 20.2 spikes/s in the 1-wk-postoperative group. No neuron was silent at rest either in the control group or in the 1-wk-postoperative group. Just after labyrinthectomy, 35% of the neurons had a null resting activity. The mean sensitivity to head velocity of these neurons was 0.55 +/- 0.42 spikes.s-1/deg.s-1 in the control group. It decreased to 0.05 +/- 0.12 spikes.s-1/deg.s-1 in the just-postoperative group and recovered to 0.22 +/- 0.17 spikes.s-1/deg.s-1 in the 1-wk-postoperative group. 8. We conclude that, at least in the guinea pig, the restoration of the spontaneous activity of the deafferented neurons is complete 1 wk after a unilateral labyrinthectomy and thus probably plays an important role in vestibular compensation...

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PubMed1994

Role of the vestibular commissure in gaze-holding in the cat: a pharmacological evaluation.

Recent theoretical studies have proposed that the vestibular commissure is a major component of the horizontal gaze-holding system. In order to test this hypothesis, we injected either bicuculline, a GABA receptor antagonist, or strychnine, a glycine receptor antagonist, into the medial vestibular nucleus of alert cats. The intervestibular connection is indeed inhibitory and mediated by GABA and glycine. As neither bicuculline nor strychnine caused serious deficit of the gaze-holding system, we conclude that the vestibular commissure is not essential for gaze-holding.

Animals↗

PubMed1994

NMDA receptors are involved in temporal integration in the oculomotor system of the cat.

Spontaneous eye movements were recorded before and after a microinjection (0.1-0.2 microliter) of either APV (an NMDA receptor antagonist) or NBQX (a non-NMDA receptor antagonist) into the nucleus prepositus hypoglossi (NPH) of the alert cat. A unilateral injection of APV caused bilateral failure of the horizontal gaze-holding system: in the light, each saccade was followed by a post-saccadic drift. A unilateral injection of NBQX caused no sign of gaze-holding failure; in the light, spontaneous eye movements were unaffected; in complete darkness, a nystagmus with linear slow phases directed towards the injected side was observed. We conclude that NMDA receptors of the NPH neurones are involved in the gaze-holding system.

2-Amino-5-phosphonovalerate↗

PubMed1994

Involvement of the N-methyl-D-aspartate receptors of the vestibular nucleus in the gaze-holding system of the cat.

Eye movements were recorded in alert cats after injections into one of the medial vestibular nuclei (MVN) either of a N-methyl-D-aspartate (NMDA) antagonist or of a non-NMDA antagonist. A gaze-holding failure was caused by the NMDA antagonist when it was injected into the central part of the MVN but not when it was injected into the rostral part of that nucleus. By contrast, injections of the non-NMDA-receptor antagonist into the MVN did not cause any sign of gaze-holding failure. We conclude that the NMDA receptors located in the central part of the MVN are involved in the gaze-holding system.

2-Amino-5-phosphonovalerate↗

PubMed1994

Cerebellar hypermetria is larger when the inertial load is artificially increased.

Hypermetria is a classical cerebellar symptom designating the overshoot observed when a patient is asked to make a very fast and accurate movement. The movement studied here was wrist flexion. Hypermetria was found to be increased by artificially increasing the inertia of the moving hand. A normal subject adapted himself to increasing inertia by increasing both his agonist activity (the launching force) and its antagonist activity (the braking force). In the same circumstances, a patient with symptoms of cerebellar system dysfunction was found to be able to increase his agonist activity but not his antagonist activity.

Acceleration↗

PubMed1994

Somatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave.

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before ("off" condition) and after a subcutaneous injection of apomorphine ("on" condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.

Aged↗

PubMed1994

Effect of muscimol microinjections into the prepositus hypoglossi and the medial vestibular nuclei on cat eye movements.

1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the nucleus prepositus hypoglossi (NPH) and the medial vestibular nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1993

The role of the vestibular commissure in the gaze holding of the cat.

Recent theoretical studies have proposed that the vestibular commissure is a major component of the horizontal gaze-holding system. In order to test this hypothesis, we disrupted the vestibular commissure of the cat by a parasagittal cut running between an abducens nucleus and the adjacent medial vestibular nucleus. Successfully lesioned cats suffered of a characteristic syndrome. In the light, gaze holding was impaired when the animal was looking toward the side of the lesion, but normal when looking toward the opposite side. We conclude (1) that the vestibular commissure is a component of the gaze-holding system, (2) that the vestibular commissure is less essential for gaze holding than other structures as the nucleus prepositus hypoglossi, and (3) that the horizontal gaze-holding system consists of two halves, each being more active in ipsilateral than in contralateral gaze.

Animals↗

PubMed1993

Testing the common neural integrator hypothesis at the level of the individual abducens motoneurones in the alert cat.

1. As far as horizontal eye movements are concerned, the well-known hypothesis of a common neural integrator states that the eye-position signal is generated by a common network, regardless of the type of versional movement. The aim of this study was to evaluate the validity of this hypothesis by analysing the behaviour of the abducens motoneurones, the system into which the horizontal neural integrator(s) project(s). If there were a common neural integrator, the different motoneurones would receive the eye position signal through the same pathway and the sensitivity to eye position would be the same regardless of the type of versional movement. If there were multiple integrators, the sensitivity to eye position in one type of versional movement might be different from the sensitivity to eye position in another type of versional movement, at least for occasional motoneurones. 2. The discharge of thirty-one antidromically identified abducens motoneurones was recorded in the alert cat during spontaneous eye movements made in the light and in response to sinusoidal rotations of the head in complete darkness. 3. All of the abducens motoneurones exhibited a burst of action potentials for lateral saccades. During fixation between saccades, they maintained a steady firing rate that increased as the cat fixated increasingly lateral eye positions. 4. For each abducens motoneurone, the sensitivity to eye position (Kf) was determined from measurements carried out during intersaccadic fixations. Kf was calculated from the slope of the firing rate-eye position linear regression line. 5. The discharge rate of the identified motoneurones was observed during four sinusoidal vestibular stimulations (+/- 10 deg, 0.10 Hz; +/- 20 deg, 0.10 Hz; +/- 30 deg, 0.10 Hz; +/- 40 deg, 0.10 Hz). The motoneurones exhibited a burst of activity during fast phases in the lateral direction and paused during fast phases in the opposite direction. During slow phases, motoneurones modulated their activity as a function of the vestibularly induced eye movements except for slow phases that occurred in position ranges below their recruitment threshold. In these cases their activity was cut off. 6. A new method was developed to measure the sensitivity to eye position of neurones during vestibular slow phases. The difficulty came from the fact that, during slow phases, eye velocity and eye position changed simultaneously and that each of those two variables could influence neuronal activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1993

Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat.

1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate. 2. Previously, microinjections of kainic acid (KA) into the region of the nucleus prepositus hypoglossi (NPH) and of the medial vestibular nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey. However, the relatively large volumes (1-3 microliters) and concentrations (2-4 micrograms microliters-1) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 microgram microliter-1) either into the rostral part of the MVN or into different sites along the NPH of the cat. 3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s. 4. In each injection experiment, the location of the abducens nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Parkinsonian bradykinesia is due to depression in the rate of rise of muscle activity.

Parkinsonian bradykinesia is defined by a slowness in the execution of movement. We studied the pathophysiology of this symptom in rapid arm-reaching movements to a visual target carried out in a reaction-time task. The major cause of bradykinesia was found to be depression in the rate of rise of electromyographic activity. The amplitude of the peak of this activity did not change significantly. There was no change either in the sequential activation of muscles, in the amount of co-contraction activity, in the accuracy of aim toward the visual target, or in the movement trajectory.

Adult↗

PubMed1992

Gaze holding defect induced by injections of ketamine in the cat brainstem.

The signal responsible for horizontal gaze holding is known to be generated, at least in part, by the prepositus hypoglossi (PH) nucleus, whereas that responsible for vertical gaze holding is known to be generated by the interstitial nucleus of Cajal (INC). An intramuscular injection of ketamine was recently demonstrated to induce a gaze holding failure. The aim of the present study was to analyse if ketamine produced this effect by acting, at least in part, on the PH nucleus. We found that a unilateral injection of a small amount of ketamine in the PH nucleus could cause either bilateral horizontal gaze holding failure or a vertical gaze holding failure or both an horizontal and a vertical gaze holding failure.

Animals↗

PubMed1990

Ketamine induces failure of the oculomotor neural integrator in the cat.

We studied the effect of intramuscular injection of low dose of ketamine (1 mg/kg) on the spontaneous ocular movements of the cat. Ketamine is a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptors, which is used as an anesthetic agent in human surgery. We found that ketamine administration caused a failure of gaze holding: each saccade was followed by a centripetal post-saccadic drift. This defect was selective: the dynamics of the saccades was not altered (the amplitude/maximum velocity relationship was unaffected by ketamine at the dose of 1 mg/kg). We postulated that the observed effect was due to the fact that NMDA receptors were implicated in the network of the oculomotor neural integrator that converted activity related to the saccade (pulse signal) into activity responsible for gaze holding (step signal).

Animals↗

PubMed1989

Eye movements evoked by microstimulations in the brainstem of the alert cat.

This study maps the eye movements evoked by microstimulations in the medulla of 9 alert cats. Trains of square waves (20 microA amplitude, 0.2 msec duration, 200 Hz) were delivered through glass-covered tungsten microelectrodes (0.5-1 M omega). Movements of both eyes were recorded by the magnetic field/eye coil technique. Stimulation of the prepositus hypoglossi nucleus (PH) evoked nystagmus with ipsilaterally-directed slow phases followed by after-nystagmus with contralaterally-directed slow phases. Stimulation of the medial vestibular nucleus (MVN) induced nystagmus whose slow phases were more often ipsilaterally-directed but at time contralaterally-directed. At nearly all sites where we stimulated the reticular formation underlying prepositus and vestibular nuclei (from P4.5 to P12), we recorded versional conjugate movements. They were most often ipsilaterally-directed. Some microstimulations in the region of the medial longitudinal fasciculus evoked recentering eye movements: regardless of the initial position of the gaze (to the left as well as to the right), microstimulations given at the same place induced a movement of both eyes toward their neutral position. The amplitude of this movement was proportional to the eccentricity of the pre-stimulation position of the gaze.

Animals↗

PubMed1988

[Contingent negative variation and regional cerebral blood flow in senile dementia and cerebral aging].

Relationships between contingent negative variation (CNV) amplitude, regional cerebral blood flow (CBF), mini mental status examination score (MMSE) and reaction time (RT) have been studied in young subjects, non-demented old subjects and patients with primary degenerative senile dementia. Significant correlations have been found between CNV amplitude and global CBF, MMSE score and reaction time. Factorial analysis has shown 3 factors weighted respectively by MMSE and CNV, antero-posterior ratio fort left hemispheric CBF and age, and antero-posterior ratio for right hemispheric CBF and reaction time. Discriminant analysis has shown 2 discriminant functions differentiating young from old subjects with 90% accuracy and demented from non-demented patients with 75% accuracy.

Adult↗

PubMed1987

Disabling of the oculomotor neural integrator by kainic acid injections in the prepositus-vestibular complex of the cat.

1. This study was intended to test the candidature of the prepositus-vestibular nuclear complex for being the location of the oculomotor neural integrator (Robinson's integrator). 2. Microinjections of kainic acid (2 micrograms dissolved in 1 microliter) were made in awake cats. Injection sites were located either in the prepositus hypoglossi nucleus (p.h.), the medial vestibular nucleus (m.v.n.), the medial longitudinal fasciculus (m.l.f.) or in the magnocellular tegmental field of the reticular formation. 3. Theory predicts that a complete disabling of the neural integrator will cause (a) an exponential post-saccadic drift whose time constant will be 0.16 s in the dark (b) a phase lead of +93 deg as the vestibulo-ocular reflex is tested at 0.10 Hz in the dark and (c) a nearly complete abolition of the optokinetic nystagmus (o.k.n.). 4. About 1 h after a unilateral kainic acid injection in the p.h., we observed (a) a large bilateral post-saccadic drift (time constant sometimes as low as 0.2 s) (b) a large phase lead at 0.10 Hz (range: from +69 to +98 deg) (c) an abolition of the o.k.n. control injection of phosphate buffer in the p.h. did not produce any deficit. 5. A unilateral kainic acid injection in the m.v.n. induced a nystagmus followed by signs of bilateral failure of the neural integrator similar to those observed after kainic acid injection in the p.h. 6. Injection near the mid-line, between the two p.h. nuclei, induced a defect of the neural integrator less than that observed after kainic acid injection in either the p.h. or the m.v.n. Injection of kainic acid in the magnocellular tegmental field of the reticular formation did not produce any sign of failure of the neural integrator. No post-saccadic drift was observed. 7. We have concluded that (a) the p.h. nucleus is involved in the integration processing, and that (b) the m.v.n. is involved either in the integration processing or in the relaying of the output of the neural integrator to the oculomotoneurones.

Animals↗

PubMed1986

Lesions in the cat prepositus complex: effects on the vestibulo-ocular reflex and saccades.

The effects of bilateral electrolytic lesions within and around the prepositus hypoglossi (p.h.) nucleus on horizontal saccades in the dark and on the horizontal sinusoidal vestibulo-ocular reflex (v.o.r.) in the dark were studied. After p.h. lesion, including its rostral part between P 7 and P 8, the v.o.r. showed a phase lead as much as about 90 deg at 0.10 Hz. A significant gain reduction paralleled that phase lead at lower frequencies. A large post-saccadic drift was also observed, the time constant of which ranged from 0.3 to 0.6 s. After p.h. lesion extending from P 8 to P 11 (but sparing the rostral part of the p.h.), no significant gain or phase lead change was observed. Post-saccadic drift was either missing or weak. A bilateral medial vestibular nucleus (m.v.n.) lesion from P 7 to P 11 produced a marked gain decrease, paralleled by a marked phase advance. A post-saccadic drift was observed (tau = 0.6 s). A surgical mid-line lesion from P 7 to P 11 (depth: about 2 mm) was followed by no remarkable change in the gain and in the phase of the v.o.r. No post-saccadic drift was observed after such lesion. It was concluded that (i) both the horizontal v.o.r. integration processing, and the horizontal saccadic integration processing were destroyed when an electrolytic lesion was made 'in the region of' the rostral part of the p.h. nucleus, and that (ii) the posterior four-fifths of the p.h. was the location of neither the horizontal v.o.r. integrator nor the horizontal saccadic integrator.

Animals↗

PubMed1986

Lesions in the cat prepositus complex: effects on the optokinetic system.

The effects of bilateral lesions within and around the prepositus hypoglossi (p.h.) nuclei on the optokinetic system were studied. The pure optokinetic nystagmus (o.k.n.) was evoked by a step of velocity (60 deg/s, 30 s duration) of the surrounding. The visual-vestibular interaction was investigated by measuring the gain and phase of the vestibulo-ocular reflex (v.o.r.) as a function of frequency before and after lesion under three different conditions of testing: basic v.o.r. tested in the dark, v.o.r. tested in the light and v.o.r. suppressed by vision. The tested amplitude was +/- 20 deg. A posterior vermectomy was performed for controls in two cats. A bilateral electrolytic p.h. lesion including the rostral pole of this nucleus was added to the posterior vermectomy in three cats. A lesion similar but sparing the rostral pole of the nucleus was carried out in three other cats. In one cat a bilateral electrolytic lesion of the medial vestibular nuclei (m.v.n.) was combined with a posterior vermectomy. In two cats the medulla was cut on the mid line after a posterior vermectomy. The posterior vermectomy affected neither the optokinetic response nor the visual-vestibular interactions. In cats where p.h. lesion included its rostral pole and in the cat with m.v.n. lesion, all the tested optokinetic effects (step o.k.n., and visual-vestibular interactions) were abolished. In the three cats where p.h. lesion spared its rostral pole, the optokinetic effects were quite normal in one cat, mildly reduced in the second one, and seriously affected but not completely abolished in the third one. The surgical cut of the medulla on the mid line did not dramatically disturb the various optokinetic effects. The most marked deficit was the loss of the optokinetic after-nystagmus (o.k.a.n.). From the comparison of these results with the neuroanatomical data and with the Robinson's model concerning the optokinetic processing, it was suggested that: (a) the rostral p.h. could be the location of the o.k.n. integrator or could be an essential link on the o.k.n. pathway, (b) the posterior four-fifths of the p.h. could not be an essential relay on the o.k.n. pathway, (c) the loss of o.k.a.n. after mid-line lesion could be due to the interruption of the positive feed-back loop formed by the reciprocal inhibitory connexions between the two m.v.n.

Animals↗