Vestibulo-oculomotor behaviour in rats following a transient unilateral vestibular loss induced by lidocaine

The effects of a transient vestibular nerve blockade, achieved by intra-tympanic instillation of lidocaine, were studied in rats by recording horizontal eye movements in darkness. Evaluation of the dose-response relationship showed that a maximal effect was attained with a concentration of 4% lidocaine. Within 15 min of lidocaine instillation, a vigorous spontaneous nystagmus was observed which reached maximal frequency and velocity of the slow phase after about 20 min. Subsequently, the nystagmus failed for approximately half an hour before it reappeared. This could be avoided by providing visual feedback in between the recordings in darkness or by a contralateral instillation of 2.5% lidocaine. It is suggested that the failure reflects an overload of the vestibulo-oculomotor circuits.

After recovery from the nerve blockade, when the gaze was stable, dynamic vestibular tests were performed. They revealed that a decrease of the slow phase velocity gain and the dominant time constant during, respectively, sinusoidal- and step stimulation toward the unanaesthetised side, had developed with the nerve blockade. These modulations were impaired by a nodulo-uvulectomy but not by bilateral flocculectomy, which is consistent with the concept of vestibular habituation.

A GABA_B receptor antagonist, CGP 56433A, given systemically during the nerve blockade, aggravated the vestibular asymmetry. The same effect has previously been demonstrated in both short- (days) and long-term (months) compensated rats, by antagonising the GABA_B receptor.

In summary, this study provides the first observations of vestibulo-oculomotor disturbances during the first hour after a rapid and transient unilateral vestibular loss in the rat. By using this method, it is possible to study immediate behavioural consequences and possible neural changes that might outlast the nerve blockade.     

Early compensation of vestibulo-oculomotor symptoms after unilateral vestibular loss in rats is related to GABA(B) receptor function

The horizontal vestibulo-oculomotor reflex was studied in pigmented rats during the first 5 days after a unilateral chemical or surgical vestibular deafferentation. Spontaneous eye movements in darkness and slow phase velocity gain of compensatory eye movements during horizontal sinusoidal rotation were evaluated. The most evident vestibulo-oculomotor symptom immediately after a unilateral vestibular loss was a spontaneous nystagmus, which gradually abated during the following days. Further, an asymmetry between ipsi- and contra-lesional gains was evident during sinusoidal vestibular stimulation. Single systemic doses of the GABA(B) receptor antagonist [3-[1-(S)-[[3-(cyclohexylmethyl)-hydroxyphosphinoyl]-2-(S)-hydroxypropyl]amino]ethyl]-benzoic acid (CGP 56433A), the agonist baclofen, or the GABA(A) receptor agonist (4,5,6,7-tetrahydroisoxazolo-[5,4-c]-pyridin-3-ol (THIP) were given at different intervals after unilateral vestibular deafferentation. CGP 56433A highly aggravated the vestibulo-oculomotor symptoms, observed as an increase in spontaneous nystagmus and slow phase velocity gain asymmetry. This effect was most pronounced during the first 2 days after unilateral vestibular loss, when CGP 56433A even decompensated the vestibular system to the extent that all vestibular responses were abolished. Baclofen caused no effect during the first days after unilateral vestibular loss, but in parallel with the abatement of spontaneous nystagmus, the drug equilibrated or even reversed the remaining spontaneous nystagmus with corresponding effects on the slow-phase velocity gain asymmetry. The effects of baclofen were very similar after both chemical and surgical deafferentation. THIP caused a slight depression of all vestibular responses. All single dose effects of the drugs were transient.Altogether these results reveal that endogenous stimulation of GABA(B) receptors in GABA-ergic vestibulo-oculomotor circuits are important for reducing the vestibular asymmetry during the early period after unilateral vestibular deafferentation. A possible role for GABA(B) receptors in the reciprocal inhibitory commissural pathways in the vestibular nuclei is suggested.     

Visual-vestibular interaction in the flocculus of the alert monkey

Summary The activity of Purkinje cells (P-cells) was recorded in the flocculus of alert Rhesus monkeys under different conditions of visual-vestibular stimulation. Stimulus conditions were vestibular, optokinetic, combined and conflicting. About 10–20% of all P-cells were activated in their simple spike activity during conflicting stimulation to the recording side (type I) and gave no response or much less during vestibular stimulation. About half of these P-cells were also activated during optokinetic stimulation to the recording side at velocities above 40–60 deg/s. Simple and complex spike activity behaved in a reciprocal way with overlapping but not identical working ranges. Simple spike modulation was unidirectional, complex spike activity always bidirectional. Modulation of simple spike activity cannot be related to one single parameter of the sensory input or the oculomotor output. The hypothesis is put forward that the vestibular nuclei and the flocculus behave in a complementary fashion in processing visual-vestibular information, the flocculus being specialized for high velocity optokinetic nystagmus and suppression of vestibular nystagmus.Supported by a grant from the Swiss National Foundation for Scientific Research 3.343-2.78     

Neurogenesis and astrogenesis contribution to recovery of vestibular functions in the adult cat following unilateral vestibular neurectomy: cellular and behavioral evidence

In physiological conditions, neurogenesis occurs in restricted regions of the adult mammalian brain, giving rise to integrated neurons into functional networks. In pathological or postlesional conditions neurogenesis and astrogenesis can also occur, as demonstrated in the deafferented vestibular nuclei after immediate unilateral vestibular neurectomy (UVN) in the adult cat. To determine whether the reactive cell proliferation and beyond neurogenesis and astrogenesis following UVN plays a functional role in the vestibular functions recovery, we examined the effects of an antimitotic drug: the cytosine-β-d arabinofuranoside (AraC), infused in the fourth ventricle after UVN. Plasticity mechanisms were evidenced at the immunohistochemical level with bromodeoxyuridine, GAD67 and glial fibrillary acidic protein (GFAP) stainings. Consequences of immediate or delayed AraC infusion on the behavioral recovery processes were evaluated with oculomotor and posturo-locomotor tests. We reported that after UVN, immediate AraC infusion blocked the cell proliferation and decreased the number of GFAP-immunoreactive cells and GABAergic neurons observed in the vestibular nuclei of neurectomized cats. At the behavioral level, after UVN and immediate AraC infusion the time course of posturo-locomotor function recovery was drastically delayed, and no alteration of the horizontal spontaneous nystagmus was observed. In contrast, an infusion of AraC beginning 3 weeks after UVN had no influence neither on the time course of the behavioral recovery, nor on the reactive cell proliferation and its differentiation. We conclude that the first 3 weeks after UVN represent a possible critical period in which important neuroplasticity mechanisms take place for promoting vestibular function recovery: reactive neurogenesis and astrogenesis might contribute highly to vestibular compensation in the adult cat.     

Flüchtiger,richtungswechselnder Spontan- und Provokationsnystagmus im Verlaufe eines Lupus erythematodes visceralis

Summary Vestibul dizziness in the course of Lupus erythematodes visceralis has not been investigated to any depth up until now. The observation of a transient, directional changing spontaneous and provoked nystagmus during an acute phase of the disease indicates that homogeneous short episodes of dizziness are probably not so rare, but the vestibular symptom, which possibly may be objectified only by Frenzel glases examination, becomes not realized or disregarded. Pathogenesis and formanalysis of nystagmus are discussed.

     

Unidirectional habituation of vestibulo-ocular responses by repeated rotational or optokinetic stimulations in the cat

Summary 1.Unilateral habituation of the vestibuloocular reflex was produced in adult cats stimulated by repeated unidirectional velocity steps (vestibular training) or by a continuously moving visual surround (optokinetic training). — 2. Unidirectional vestibular training produced a strong asymmetry of vestibuloocular responses (VOR). Responses to velocity steps applied to the trained labyrinth were decreased both in gain and in time-constant. This effect generalized to responses to sinusoidal oscillations (0.03 Hz to 0.1 Hz), i.e. to a stimulus not used during training. — No spontaneous nystagmus was ever observed in spite of the dynamic VOR asymmetry. — 3. Unilateral vestibular habituation produced by vestibular training appeared to be a long-lasting phenomenon. It was still present 10 days after the end of training. — 4. Optokinetic responses were not affected by vestibular training. — 5. Unidirectional optokinetic training produced an increase in the slow phase velocity of optokinetic nystagmus (OKN) by about 25% in both directions. This effect did not persist for more than a few minutes. A marked spontaneous nystagmus was recorded in the dark after each session of optokinetic training, with a slow phase in the direction opposite to the previous OKN. — 6. VOR in response to velocity steps and to sinusoidal oscillations were decreased unilaterally after optokinetic training. This effect was of short duration, however, and disappeared within the interval between training sessions. This lack of retention contrasted with the prolonged effect of vestibular training.Supported by INSERM (France) and by CNR (Italy)     

Effects of cosmonaut vestibular training on vestibular function prior to spaceflight

The purpose of this study was to quantify the effects of repetitive Coriolis and cross-coupled stimulations, similar to the vestibular training the cosmonauts are exposed to prior to their spaceflight, on vestibular function in control subjects on Earth. Ten volunteers were passively rotated in yaw on a rotating chair while executing standardized pitch head-and-trunk movements. The chair stopped to change direction after 12 head-and-trunk movements were made. The runs were grouped in sessions of ten,which were repeated daily for 10 days. The severity of motion sickness was assessed by subjective judgment and measurements of skin pallor and salivary total protein concentration, and nystagmus was recorded. The severity of motion sickness and nystagmus decreased during cosmonaut vestibular training (CVT). One month after the end of CVT, nystagmus responses were still about 20–30% lower than control values. These results indicate that CVT induces a habituation of vestibular responses. One important implication of this experiment concerns space studies on cosmonauts who are exposed to such vestibular training prior to their spaceflight. Electronic Publication     

Circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesia in the rabbit

1. The effects of chloralose-urethane and sodium pentobarbitone anaesthesia on heart rate, blood pressure and cardiac output were studied in normal rabbits, in animals given atropine and in animals without functioning autonomic effectors. The findings under anaesthesia were compared during spontaneous and artificial intermittent positive pressure respiration.2. The circulatory effects of chloralose-urethane and sodium pentobarbitone anaesthesia differed significantly for the first hour after induction of anaesthesia. During the subsequent 3 hr of maintained anaesthesia differences in the circulatory effects of the two anaesthetics were small.3. The direct local effects of these anaesthetics were assessed during the maintenance phase from the responses of animals without functioning autonomic effectors. With both anaesthetics there was peripheral vasodilatation and minimal effects on heart rate.4. The autonomic activity in the normal animal was assessed by comparing the changes in normal, atropinized and ;de-efferented' rabbits without functioning autonomic effectors. During chloralose-urethane anaesthesia there was reduction in cardiac vagal efferent activity and no change in cardiac sympatho-adrenal activity. With both anaesthetics there was an increase in peripheral sympatho-adrenal constrictor activity, tending to minimize the local vasodilator effects.     

Injections of calmidazolium chloride into the ipsilateral medial vestibular nucleus or fourth ventricle reduce spontaneous ocular nystagmus following unilateral labyrinthectomy in guinea pigs

The effects of three injections (0.5–4.5 h postoperation) of 1-[bis-(p-chlorophenyl)methyl]-3-[2,4-dichloro-beta-(2, 4-dichlorobenzyloxy)phenethyl]-imidazolium chloride (calmidazolium chloride, R24571), into the ipsilateral medial vestibular nucleus or fourth ventricle, on vestibular compensation for unilateral labyrinthectomy was studied in guinea pigs. R24571, a calmodulin antagonist and inhibitor of several Ca²⁺-dependent enzymes, caused a significant reduction in the average frequency of spontaneous ocular nystagmus (spontaneous nystagmus) during the first 53 h following unilateral labyrinthectomy (n= 5), compared with vehicle-injected animals (n=5). Although a statistical analysis was not performed on the yaw head tilt and roll head tilt data because of the large variability between animals over the 53-h period of compensation, most R24571 treated animals had less yaw head tilt (4/4 animals) and roll head tilt (4/5 animals) at 9–11 h post-labyrinthectomy than the average values for the vehicle groups at that time. The decrease in the frequency of spontaneous nystagmus following R24571 treatment was not associated with general ataxia or sedation. These results are consistent with recent biochemical studies in suggesting that intracellular pathways associated with Ca²⁺ may be involved in the neuronal mechanisms of vestibular compensation following unilateral labyrinthectomy.     

Vestibular nuclei activity during optokinetic after-nystagmus (OKAN) in the alert monkey

Summary Neurons which receive an input from the horizontal semicircular canals were recorded from the vestibular nuclei in chronically prepared monkeys (Macaca mulatta) during optokinetic after-nystagmus (OKAN). In complete darkness the vestibular neurons showed activity changes which closely paralleled the strength of nystagmus. The activity of vestibular units returned to baseline levels of spontaneous discharge only when all after-nystagmus had ceased, or when it was inhibited by stationary visual stimuli. The possible role of vestibular neurons in the generation of OKAN and its significance in vestibulo-visual interaction is discussed.Supported in part by Swiss National Foundation for Scientific Research 3.672-0.77 and Emil Barell-Foundation of Hoffman-La Roche, Basel, Switzerland     

Horizontal eye position-related activity in neck muscles of the alert cat

Summary The activity of neck muscles was recorded in the alert, head-fixed cat together with the horizontal and vertical components of eye movements. Electromyographic activity of obliquus capitis cranialis and caudalis, and longissimus capitis, is closely related to horizontal eye position in the orbit both during spontaneous eye movements and vestibular nystagmus. The activity of splenius also shows this relationship but the coupling is less tight, probably because of the postural function of this muscle.Supported by INSERM PRC grant no. 50-7723     

A comparison of the transient hyperprolactinaemic stress response obtained using two different methods of analgesia for ultrasound-guided transvaginal oocyte retrieval.

Transient hyperprolactinaemia has been shown to accompany the procedure of oocyte retrieval under laparoscopic control. This study was concerned with establishing whether transvaginal oocyte retrieval was also associated with hyperprolactinaemia and whether the hyperprolactinaemic response was dependent on the method of anaesthesia/analgesia employed. Two distinct patterns were recorded. Oocyte retrieval under general anaesthesia was accompanied by a rapid rise in prolactin levels, which peaked after 40 min. Oocyte retrieval under intravenous sedation was associated with a slow rise in circulating prolactin concentrations. Significant differences in the prolactin rise between the general anaesthesia and sedation groups appeared within 10 min of the start of the procedure. It is concluded that although the surgical stress of oocyte recovery is associated with mild transient hyperprolactinaemia, most of the hyperprolactinaemic response is due to the anaesthetic.     

Vestibular nerve activity in the alert monkey during vestibular and optokinetic nystagmus

Summary Activity of vestibular nerve fibers and eye movements were recorded in the alert monkey during natural stimulation. The animal was rotated about a vertical axis in the dark with velocity trapezoids (vestibular), or a striped cylinder was rotated around the stationary monkey (optokinetic), or these stimuli were combined.After velocity steps in the dark, neuronal activity declined with a dominant time constant of 5–6 s. The time constant of nystagmus recorded simultaneously was always longer, on average 23 s. Vestibular nerve activity was not influenced by optokinetic patterns or additional visual stimuli during combined visualvestibular stimulation. Thus, in contrast to vestibular nuclei neurons, vestibular nerve activity in the alert monkey is only determined by head acceleration and cannot be related to the nystagmus response or visual stimuli.Supported by a grant from the Swiss National Foundation for Scientific Research 3.343-2.78     

Role of irregular otolith afferents in the steady-state nystagmus during off-vertical axis rotation.

1. During constant velocity off-vertical axis rotations (OVAR) in the dark a compensatory ocular nystagmus is present throughout rotation despite the lack of a maintained signal from the semicircular canals. Lesion experiments and canal plugging have attributed the steady-state ocular nystagmus during OVAR to inputs from the otolith organs and have demonstrated that it depends on an intact velocity storage mechanism. 2. To test whether irregularly discharging otolith afferents play a crucial role in the generation of the steady-state eye nystagmus during OVAR, we have used anodal (inhibitory) currents bilaterally to selectively and reversibly block irregular vestibular afferent discharge. During delivery of DC anodal currents (100 microA) bilaterally to both ears, the slow phase eye velocity of the steady-state nystagmus during OVAR was reduced or completely abolished. The disruption of the steady-state nystagmus was transient and lasted only during the period of galvanic stimulation. 3. To distinguish a possible effect of ablation of the background discharge rates of irregular vestibular afferents on the velocity storage mechanism from specific contributions of the dynamic responses from irregular otolith afferents to the circuit responsible for the generation of the steady-state nystagmus, bilateral DC anodal galvanic stimulation was applied during optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN). No change in OKN and OKAN was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-volatile general anaesthetics reduce spinal activity by suppressing plateau potentials

Non-volatile general anaesthetics are thought to reduce brain activity by potentiating inhibitory GABA(A) receptor channels but also cause adverse effects by suppress ing L-type calcium channels in the heart. In sections of the spinal cord, the non-volatile anaesthetics pentobarbital, thiopental and propofol reduced excitability of sensorimotor neurons by suppressing plateau potentials mediated by L-type calcium channels. This effect was independent of GABA(A) receptor potentiation but occurred in an overlapping concentration range. Therefore, the suppressive effect of non-volatile anaesthetics on L-type calcium channels can contribute to the reduction of spinal sensorimotor activity during anaesthesia. The results support the idea that general anaesthesia is achieved through several mechanisms and suggest that procedures for anaesthesia may be improved by combining selective agents for each mechanism in optimal concentrations.     

Visual-vestibular interactions during vestibular compensation: role of the pretectal not in horizontal VOR recovery after hemilabyrinthectomy in rhesus monkey

Damage to the vestibular labyrinth leads to profound nystagmus and vertigo. Over time, the vestibular-ocular system recovers in a process called vestibular compensation leading to reduced nystagmus and vertigo provided visual signals are available. Our study was directed at identifying sources of visual information that could play a role in vestibular compensation. Specifically, we investigated the role of the pretectal nucleus of the optic tract (NOT) in vestibular compensation after hemilabyrinthectomy (HL) in rhesus monkeys. We chose the NOT because this structure provides critical visual motion information for adaptive modification of the vestibular ocular reflex (VOR). We produced bilateral NOT lesions by injecting the excitotoxin ibotenic acid. We compared vestibular compensation after HL in NOT-lesioned and control animals with intact NOTs. We measured eye movements with an electromagnetic method employing scleral search coils. Measurements included slow-phase eye velocity during spontaneous nystagmus, per- and postrotatory nystagmus and the horizontal VOR (hVOR) gain (eye-velocity/head velocity) associated with per- and postrotatory and sinusoidal (0.2-2.0 Hz; 30-90 degrees/s) whole body oscillation around the earth-vertical axis. VOR gain was low (<0.5) for rotation toward the HL side. Our control animal evinced significant vestibular compensation with VOR gains approaching unity by 100 days post HL. In contrast, monkeys with bilateral lesions of the NOT never obtained this significant recovery with hVOR gains well below unity at 100 days and beyond. Therefore our studies demonstrate that the NOT is an essential source of visual signals for the process of vestibular compensation after HL.     

Plastic changes underlying vestibular compensation in the guinea-pig persist in isolated, in vitro whole brain preparations.

Vestibular compensation for the postural and oculomotor deficits induced by unilateral labyrinthectomy is a model of post-lesional plasticity in the central nervous system. Just after the removal of one labyrinth, the deafferented, ipsilateral vestibular nucleus neurons are almost silent, and the discharge of the contralateral vestibular nucleus neurons is increased. The associated static disorders disappear in a few days, as normal activity is restored in both vestibular nuclei. In this study, we searched for traces of vestibular compensation in isolated whole brains taken from adult guinea-pigs. The electrophysiological responses evoked in control brains were compared to those evoked in brains taken from animals that had previously been labyrinthectomized. Guinea-pigs compensated for an initial labyrinthectomy within three days. In vivo, subsequent deafferentation of vestibular nucleus neurons on the intact side triggered "Bechterew's phenomenon": a new postural and oculomotor syndrome appeared, similar to the one induced by the first lesion, but directed to the newly deafferented side. These disturbances would be caused by the new imbalance between the discharges of neurons in the two vestibular nuclei triggered by the second deafferentation. Experiments were designed to search for a similar imbalance in vitro in brains taken from labyrinthectomized animals, where the intact vestibular nerve is cut during the dissection. Isolated whole brains were obtained from young guinea-pigs at various times (one to seven days) following an initial labyrinthectomy. An imbalance between the resting activities of medial vestibular nucleus neurons on both sides of the brainstem was revealed in brains taken more than three days after the lesion: their discharge was higher on the compensated, initially lesioned side than on the newly deafferented side. In some cases, an oscillatory pattern of discharge, reminiscent of the spontaneous nystagmus associated in vivo with Bechterew's syndrome, appeared in both abducens nerves. These data demonstrate that most of the changes underlying vestibular compensation persist, and can thus be investigated in the isolated whole brain preparation. Brains removed only one day after the lesion displayed normal commissural responses and symmetric spinal inputs to vestibular nucleus neurons. However, an unusually large proportion of the neurons recorded on both sides of the preparation had very irregular spontaneous discharge rates. These data suggest that the first stages of vestibular compensation might be associated with transient changes in the membrane properties of vestibular nucleus neurons. Brains taken from compensated animals displayed a significant, bilateral decrease of the inhibitory commissural responses evoked in the medial vestibular nucleus by single-shock stimulation of the contralateral vestibular nerve. The sensitivity of abducens motoneurons on the initially lesioned, compensated side to synaptic activation from the contralesional vestibular nucleus neurons was also decreased. Both changes may explain the long-term, bilateral decrease of vestibular-related reflexes observed following unilateral labyrinthectomy. Spinal inputs to vestibular nucleus neurons became progressively asymmetric: their efficacy was increased on the lesioned side and decreased on the intact one. This last modification may support a functional substitution of the deficient, vestibular-related synergies involved in gaze and posture stabilization by neck-related reflexes.     

Velocity storage in the vestibulo-ocular reflex arc (VOR)

Summary Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 °/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 °/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression).These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.     

Analysis of vertebrate eye movements following intravitreal drug injections. II. Spontaneous nystagmus induced by picrotoxin is mediated subcortically

1. Eye movements were observed following an injection of picrotoxin, a GABA antagonist, into the vitreous of one eye. A spontaneous nystagmus was observed in cats, rabbits, and turtles, even in total darkness, with slow-phase eye movements in the temporal-to-nasal direction for the injected eye. 2. During visual stimulation by a horizontal drifting pattern, injected eyes moved in the temporal-to-nasal direction, irrespective of stimulus direction. In cats, however, the nystagmus was usually slower when the injected eye viewed nasal-to-temporal motion (opposite to the direction of the spontaneous nystagmus). The spontaneous nystagmus could be halted or even reversed by allowing cats to view motion opposite to the direction of the nystagmus with the uninjected eye alone. The nystagmus could not be overridden in this fashion in rabbits or turtles. 3. The nystagmus induced by picrotoxin could also be modified by vestibular stimulation. When cats were placed on their sides, the spontaneous horizontal nystagmus often decreased and spontaneous vertical nystagmus with upward slow phase movements occurred. During sinusoidal horizontal vestibular stimulation, the horizontal nystagmus due to picrotoxin added to the vestibuloocular reflex as a velocity offset in the temporal-to-nasal direction. 4. Following bilateral ablation of the cat visual cortex, picrotoxin's effect became even more pronounced than before the ablation. Therefore, at least some picrotoxin-sensitive cells can use subcortical pathways, perhaps to the accessory optic nuclei. The visual cortex, which also processes directional information, may be able to compensate for changes in retinal processing induced by picrotoxin in intact animals. 5. This study demonstrates the importance of retinal GABA in the control of eye stability. As GABA is known to be responsible for null direction inhibition of directionally sensitive retinal ganglion cells, these results suggest that the output of these cells may be critical for the normal functioning of central optokinetic pathways, even in the absence of visual cortex.     

Two stages of excitability change of pontine pause neurons in the cat

Spikes of single pontine pause neurons (PNs) in the cat were recorded extracellularly and identified by observing cessation of tonic discharges before and during the fast phase of vestibular nystagmus. PNs were antidromically activated from the excitatory burst neuron area. Antidromic spikes were abolished or their peak latencies were prolonged during particular periods within a nystagmic cycle. The excitability change in PNs indicated by alteration of the antidromic responses occurred with two stages; i.e. a moderate decrease in excitability before the onset of the fast phase and an abrupt, intense decrease starting form the beginning of the fast phase.