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C de Waele

Publications and source records attributed to C de Waele.

At least 19 recordsLinked to original sources
PubMed2006

Modulation of inhibitory and excitatory synaptic transmission in rat inferior colliculus after unilateral cochleectomy: an in situ and immunofluorescence study.

We investigated whether inhibitory synaptic transmission mediated through glycinergic receptor, GABAA receptors, glutamic acid decarboxylase, the enzyme synthesizing GABA, and excitatory synaptic transmission through alpha-amino-3-hydroxi-5-methylisoxazole-4-propionic acid receptors and N-methyl-D-aspartate receptors are affected in the inferior colliculus by unilateral surgical cochleectomy. In situ hybridization and immunohistofluorescence studies were performed in normal and lesioned adult rats at various times following the lesion (1-150 days). Unilateral auditory deprivation decreased glycine receptor alpha1 and glutamic acid decarboxylase 67 expression in the contralateral central nucleus of the inferior colliculus. This decrease began one day after cochleectomy, and continued until day 8; thereafter expression was consistently low until day 150. The glycine receptor alpha1 subunit decrease did not occur if a second contralateral cochleectomy was performed either on day 8 or 150 after the first cochleectomy. Bilateral cochleectomy caused also a bilateral inferior colliculus diminution of glutamic acid decarboxylase 67 mRNA at post-lesion day 8 but there were no changes in glycine receptor alpha1 compared with controls. In contrast, the abundance of other alpha2-3, and beta glycine receptor, gephyrin, the anchoring protein of glycine receptor, the alpha1, beta2 and gamma2 subunits of GABAA receptors, GluR2, R3 subunits of alpha-amino-3-hydroxi-5-methylisoxazole-4-propionic acid receptors, and NR1 and NR2A transcripts of N-methyl-D-aspartate receptors was unaffected during the first week following the lesion. Thus, unilateral cochlear removal resulted in a selective and long-term decrease in the amount of the glycine receptor alpha1 subunit and of glutamic acid decarboxylase 67 in the contralateral central nucleus of the inferior colliculus. These changes most probably result from the induced asymmetry of excitatory auditory inputs into the central nucleus of the inferior colliculus and may be one of the mechanisms involved in the tinnitus frequently encountered in patients suffering from a sudden hearing loss.

Animals↗
PubMed2005

Modulation of the glutamatergic receptors (AMPA and NMDA) and of glutamate vesicular transporter 2 in the rat facial nucleus after axotomy.

Facial nerve axotomy is a good model for studying neuronal plasticity and regeneration in the peripheral nervous system. We investigated in the rat the effect of axotomy on the different subunits of excitatory glutamatergic AMPA (GLuR1-4), NMDA (NR1, NR2A-D) receptors, post-synaptic density 95, vesicular glutamate transporter 2, beta catenin and cadherin. mRNA levels and/or protein production were analyzed 1, 3, 8, 30 and 60 days after facial nerve axotomy by in situ hybridization and immunohistofluorescence. mRNAs coding for the GLuR2-4, NR1, NR2A, B, D subunits of glutamatergic receptors and for post-synaptic density 95, were less abundant after axotomy. The decrease began as early as 1 or 3 days after axotomy; the mRNAs levels were lowest 8 days post-lesion, and returned to normal or near normal 60 days after the lesion. The NR2C subunit mRNAs were not detected in either lesioned or intact facial nuclei. Immunohistochemistry using specific antibodies against GLuR2-3 subunits and against NR1 confirmed this down-regulation. There was also a large decrease in vesicular glutamate transporter 2 immunostaining in the axotomized facial nuclei at early stages following facial nerve section. In contrast, no decrease of NR2A subunit and of post-synaptic density 95 could be detected at any time following the lesion. beta Catenin and cadherin immunoreactivity pattern changed around the cell body of facial motoneuron by day 3 after axotomy, and then, tends to recover at day post-lesion 60 days. Therefore, our results suggest a high correlation between restoration of nerve/muscle synaptic contact, synaptic structure and function in facial nuclei. To investigate the mechanisms involved in the change of expression of these proteins following axotomy, the facial nerve was perfused with tetrodotoxin for 8 days. The blockade of action potential significantly decreased GLuR2-3, NR1and NR2A mRNAs in the ipsilateral facial nuclei. Thus, axotomy-induced changes in mRNA abundance seemed to depend partly on disruption of activity.

Animals↗
PubMed2005

Postural control in patients with unilateral vestibular lesions is more impaired in the roll than in the pitch plane: a static and dynamic posturography study.

The postural instability of patients with vestibular loss (11 with bilateral and 101 with unilateral vestibular loss) at different times following the lesion was investigated by means of posturography and compared to healthy subjects. In addition, subjects submitted to galvanic vestibular stimulation were also studied to compare their postural performances with those of patients with complete unilateral vestibular lesion. The platform consisted of a static computerized force platform, on which a seesaw platform could be placed to test the subjects in dynamic conditions. The displacement of the center of foot pressure was measured under different conditions: subjects standing on the fixed platform, eyes open and eyes closed and subjects standing on the seesaw platform, eyes open and eyes closed. In the last condition, balance was tested in the subject's pitch plane by allowing the platform to rotate forwards and backwards only and in the patient's roll plane by allowing the platform to rotate to the left and to the right. The results showed that in static conditions, only bilateral vestibular loss patients had abnormal values compared to controls. In contrast, in dynamic eyes-closed conditions, both bilateral and unilateral patients could be differentiated from controls. Bilateral patients were unable to stand up without falling in both pitch and roll planes. Unilateral patients fell in the first week following the lesion and exhibited increased postural oscillations in both planes from the 2-week up to the 1-year postlesion stage. In addition and more importantly, they fell more often or had higher sway in the roll than in the pitch plane. Therefore, this study suggests that dynamic posturography on a seesaw platform could be a valuable tool for clinical diagnosis and quantitative analysis of imbalance in patients suffering from a unilateral vestibular loss up to 1 year after the lesion.

Accidental Falls↗
PubMed2005

The differential response of astrocytes within the vestibular and cochlear nuclei following unilateral labyrinthectomy or vestibular afferent activity blockade by transtympanic tetrodotoxin injection in the rat.

In this study, we investigated whether changes in the vestibular neuronal activity per se influence the pattern of astrocytes morphology, glial fibrillary acidic protein (GFAP) expression and ultimately their activation within the vestibular nuclei after unilateral transtympanic tetrodotoxin (TTX) injections and after unilateral inner ear lesion. The rationale was that, theoretically the noninvasive pharmacological functional blockade of peripheral vestibular inputs with TTX, allowed us to dissociate the signals exclusively related to the shutdown of the resting activity of the first-order vestibular neurons and from neuronal signals associated with trans-ganglionic changes in first order vestibular neurons induced by unilateral labyrinthectomy (UL). Since the cochlea was removed during the surgical procedure, we also studied the astrocytic reaction within the deafferented cochlear nuclei. No significant changes in the distribution or relative levels of GFAP mRNA expression, relative levels of GFAP protein or immunoreactivity for GFAP were found in the ipsilateral vestibular nuclei at any post-TTX injection times studied. In addition, no sign of microglia activation was observed. In contrast, a robust increase of the distribution and relative levels of GFAP mRNA expression, protein levels and immunoreactivity was observed in the deafferented vestibular and cochlear nuclei beginning at 1 day after inner ear lesion. GFAP mRNA expression and immunoreactivity in the cochlear nucleus was qualitatively stronger than in the ipsilateral vestibular nuclei. The results suggest that astrocyte activation in the vestibular nuclei is not related to drastic changes of vestibular nuclei neuronal activity per se. Early trans-ganglionic changes due to vestibular nerve dendrites lesion provoked by the mechanical destruction of vestibular receptors, most probably induced the glial reaction. Its functional role in the vestibular compensation process remains to be elucidated.

Afferent Pathways↗
PubMed2003

Modulation of the beta1-3 voltage-gated sodium channels in rat vestibular and facial nuclei after unilateral labyrinthectomy and facial nerve section: an in situ hybridization study.

We investigated whether the production of the mRNAs for the auxiliary beta subunits of the Na channels are modulated in deafferented medial vestibular nucleus (MVN) and in axotomized facial motoneurons. No beta1-3 mRNAs modulation was detected at any time following unilateral labyrinthectomy in the deafferented and intact medial vestibular nucleus. In contrast, beta1 gene expression in the axotomized facial nucleus decreased compared to controls as soon as day post-lesion 3.

Animals↗
PubMed2002

GluR2-R4 AMPA subunit study in rat vestibular nuclei after unilateral labyrinthectomy: an in situ and immunohistochemical study.

In the present investigation, we address the question of whether the expression of GluR2-R4 subunits mRNAs and GluR2 and GluR4 subunits protein of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)-selective glutamate receptors are modulated in the vestibular nuclei following unilateral labyrinthectomy. Specific GluR2-R4 radioactive oligonucleotides were used to probe sections of rat vestibular nuclei according to in situ hybridization methods. The signal was detected by means of film or emulsion photography. GluR2 and GluR4 subunit expression were also measured in control and operated rats by use of specific monoclonal GluR2 and GluR4 antibodies. Animals were killed at different stages following the lesion: 1, 3 or 8 days for the in situ hybridization study and 4 and 8 days for the immunohistochemical study. In normal animals, several brainstem regions including the lateral, medial, superior and inferior vestibular nuclei expressed all the GluR2, GluR3 and GluR4 subunit mRNAs. Moreover, numerous vestibular nuclei neurons are endowed with AMPA receptors containing the GluR2 and the GluR4 subunits. In unilaterally labyrinthectomized rats, no asymmetry could be detected on autoradiographs between the two medial vestibular nuclei probed with the GluR2 and the GluR4 oligonucleotide probes regardless of the delay following the lesion. However, compared to control, a bilateral decrease (-22%) in GluR3 gene expression was observed in the medial vestibular nuclei 3 days after the lesion followed by a return to normal at day 8 post-lesion. No significant asymmetrical changes in the density of GluR2- and GluR4-immunopositive cells could be detected between the intact and deafferented sides in any part of the vestibular nuclear complex and at any times (day 4 or day 8) following the lesion. Our data show that the removal of glutamatergic vestibular input induced an absence of modulation of GluR2 and GluR4 gene and subunits expression. This demonstrates that GluR2 and GluR4 expression do not play a role in the recovery of the resting discharge of the deafferented medial vestibular nuclei neurons and consequently in the functional restoration of the static postural and oculomotor deficits. The functional role of the slight and bilateral GluR3 mRNA decrease in the vestibular nuclei remains to be elucidated.

Animals↗
PubMed2001

Vestibular projections in the human cortex.

There is considerable evidence from studies on cats and monkeys that several cortical areas such as area 2v at the tip of the intraparietal sulcus, area 3av in the sulcus centralis, the parietoinsular vestibular cortex adjacent to the posterior insula (PIVC) and area 7 in the inferior parietal lobule are involved in the processing of vestibular information. Microelectrode recordings from these areas have shown that: (1) most of these cortical neurons are connected trisynaptically to the labyrinthine endorgans and (2) they receive converging vestibular, visual and somatosensory inputs. These data suggest that a multimodal cortical system is involved in postural and gaze control. In humans, recent positron emission tomography (PET) scans and functional magnetic resonance imaging (fMRI) studies have largely confirmed these data. However, because of the limited temporal resolution of these two methods, the minimum time of arrival of labyrinthine inputs from the vestibular hair cells to these cortical areas has not yet been determined. In this study, we used the evoked potential method to attempt to answer this question. Due to its excellent temporal resolution, this method is ideal for the investigation of the tri- or polysynaptic nature of the vestibulocortical pathways. Eleven volunteer patients, who underwent a vestibular neurectomy due to intractable Meniere's disease (MD) or acoustic neurinoma resection, were included in this experiment. Patients were anesthetized and the vestibular nerve was electrically stimulated. The evoked potentials were recorded by 30 subcutaneous active electrodes located on the scalp. The brain electrical source imaging (BESA) program (version 2.0, 1995) was used to calculate dipole sources. The latency period for the activation of five distinct cortical zones, including the prefrontal and/or the frontal lobe, the ipsilateral temporoparietal cortex, the anterior portion of the supplementary motor area (SMA) and the contralateral parietal cortex, was 6 ms. The short latency period recorded for each of these areas indicates that several trisynaptic pathways, passing through the vestibular nuclei and the thalamic neurons, link the primary vestibular afferents to the cortex. We suggest that all these areas, including the prefrontal area, process egomotion information and may be involved in planning motor synergies to counteract loss of equilibrium.

Brain Mapping↗
PubMed2001

Variability in the control of head movements in seated humans: a link with whiplash injuries?

The aim of this study was to determine how context and on-line sensory information are combined to control posture in seated subjects submitted to high-jerk, passive linear accelerations. Subjects were seated with eyes closed on a servo-controlled linear sled. They were asked to relax and received brief accelerations either sideways or in the fore-aft direction. The stimuli had an abrupt onset, comparable to the jerk experienced during a minor car collision. Rotation and translation of the head and body were measured using an Optotrak system. In some of the subjects, surface electromyographic (EMG) responses of selected neck and/or back muscles were recorded simultaneously. For each subject, responses were highly stereotyped from the first trial, and showed little sign of habituation or sensitisation. Comparable results were obtained with sideways and fore-aft accelerations. During each impulse, the head lagged behind the trunk for several tens of milliseconds. The subjects' head movement responses were distributed as a continuum in between two extreme categories. The 'stiff' subjects showed little rotation or translation of the head relative to the trunk for the whole duration of the impulse. In contrast, the 'floppy' subjects showed a large roll or pitch of the head relative to the trunk in the direction opposite to the sled movement. This response appeared as an exaggerated 'inertial' response to the impulse. Surface EMG recordings showed that most of the stiff subjects were not contracting their superficial neck or back muscles. We think they relied on bilateral contractions of their deep, axial musculature to keep the head-neck ensemble in line with the trunk during the movement. About half of the floppy subjects displayed reflex activation of the neck muscles on the side opposite to the direction of acceleration, which occurred before or during the head movement and tended to exaggerate it. The other floppy subjects seemed to rely on only the passive biomechanical properties of their head-neck ensemble to compensate for the perturbation. In our study, proprioception was the sole source of sensory information as long as the head did not move. We therefore presume that the EMG responses and head movements we observed were mainly triggered by the activation of stretch receptors in the hips, trunk and/or neck. The visualisation of an imaginary reference in space during sideways impulses significantly reduced the head roll exhibited by floppy subjects. This suggests that the adoption by the central nervous system of an extrinsic, 'allocentric' frame of reference instead of an intrinsic, 'egocentric' one may be instrumental for the selection of the stiff strategy. The response of floppy subjects appeared to be maladaptive and likely to increase the risk of whiplash injury during motor vehicle accidents. Evolution of postural control may not have taken into account the implications of passive, high-acceleration perturbations affecting seated subjects.

Acceleration↗
PubMed2001

Abnormal vestibular control of gaze and posture in a strain of a waltzing rat.

The waltzing behavior is usually attributed to vestibular dysfunction. However, the vestibular control of gaze and posture has not yet been measured quantitatively in any waltzing mutant. Therefore, this study was aimed at investigating the relationship between inner-ear morphology, the circling behavior, and the vestibular control of gaze and posture in a new strain of waltzing rats. Light- and electron-microscopy studies of these mutants did not reveal any structural abnormalities of the vestibular neural epithelia. In addition, the expression of Calretinin and 200-kD phosphorylated and non-phosphorylated neurofilaments was also found to be normal in the vestibular neural epithelia and ganglion cells. In contrast, the mutants showed severe dysfunctions of the vestibular control of gaze and posture. The skeletal geometry of the alert unrestrained animals was studied using cineradiography. At rest, waltzing rats held their heads tilted down: the horizontal semicircular-canal's plane was near the earth-horizontal's plane, instead of being tilted up as in Long Evans control rats. In addition, their cervical column was pitched more forward (33.6 degrees) than in the control group (6.9 degrees). The circling behavior was observed frequently, and the rats had episodes of circling in both directions. The episodes of circling amounted to an average of 17 turns, and the average angular velocity of the circling was 645 degrees/s. Unilateral labyrinthectomy induced the same postural and oculomotor syndromes in the waltzing and control groups. This indicates that the mutant vestibular nerve had a significant resting discharge before the lesion. Eye movements were recorded using acutely implanted search coils. Although waltzing rats were able to perform normal spontaneous eye movements, they showed a complete deficit of the horizontal vestibulo-ocular reflex (HVOR) and an impairment of the maculo-ocular reflex (MOR) during constant velocity, off-vertical axis rotation (OVAR). These results show, for the first time, that deficient transduction and/or processing of the horizontal-canal- and macular-related information can be causally related to the circling behavior and abnormal posture, respectively.

Animals↗
PubMed2000

Lack of growth-associated protein-43 reemergence or of growth-associated protein-43 mRNA modulation in deafferented vestibular nuclei during the first 6 weeks after unilateral inner ear lesion.

We investigated whether a unilateral inner ear lesion that destroyed the labyrinthine receptors, the cochlear receptors, and the spiral ganglion induced collateral sprouting in rat vestibular and auditory brainstem nuclei, using growth-associated protein-43 (GAP-43) as an indicator of synaptic remodeling. Both immunocytochemistry and in situ hybridization were performed to detect a potential modulation of GAP-43 and of its messenger RNA (mRNA) at different times after surgery. We failed to observe a reemergence of GAP-43 or a modulation of its mRNA in the deafferented vestibular nuclei at all survival times tested. In contrast, a substantial increase in the expression of GAP-43 was observed in the neuropil of the ipsilateral deafferented cochlear nuclei and in cell bodies of the ipsilateral superior olive. This increase was associated with an up- and downregulation of the mRNA coding for GAP-43 in the ipsilateral ventral cochlear nucleus and in the ipsilateral superior olive, respectively. These data indicate that synaptic remodeling, as assessed by GAP-43 expression, does not seem to occur in the deafferented vestibular complex during the first 6 weeks after labyrinthectomy, whereas it occurs within the first deafferented auditory relays at times as early as 4 days following spiral ganglion and cochlear receptors removal. We conclude that recovery of a normal resting discharge of the deafferented central vestibular neurons and consequently recovery of a normal resting posture and eye position may not depend on collateral sprouting of the remaining vestibular afferents. In contrast, we confirmed that a reactive synaptogenesis occurs in the brainstem auditory nuclei following cochlea and spiral ganglion removal. Its functional significance remains an open question.

Afferent Pathways↗
PubMed1999

Neck muscle activity after unilateral labyrinthectomy in the alert guinea pig.

In the guinea pig, lateral deviation of the head is a cardinal symptom of the vestibular syndrome caused by unilateral labyrinthectomy. In the course of recovery from this syndrome (vestibular compensation), lateral deviation of the head disappears completely in 2-3 days. Because this symptom is known to be due to the lesion of the horizontal semicircular canal system, and since obliquus capitis inferior (OCI) muscle is activated predominantly by yaw rotation (horizontal vestibulocollic reflex), we hypothesized that changes in the activity of this muscle could be at least in part responsible for the lateral head deviation caused by unilateral labyrinthectomy. In order to test this hypothesis, electromyographic (EMG) activities of the right and left OCI muscles, as well as eye movements, were recorded in 12 head-fixed alert guinea pigs at various times after left surgical labyrinthectomy (performed with the animals under halothane anesthesia). After the operation, a decrease in tonic EMG activity was observed in the right (contralateral to the lesion) OCI muscle while an increase in tonic EMG activity was detected in the left (ipsilateral) OCI muscle. In addition, phasic changes in EMG activity associated with ocular nystagmic beats occurred in the OCI muscles. These phasic changes were in the opposite direction to those of the tonic changes. There were bursts of activity in the right OCI and pauses in the left OCI. From measurements of rectified averaged EMG activities which took into account both parts (tonic and phasic) of the phenomenon, it was concluded that the labyrinthectomy-induced asymmetry between the activities of the left and right OCI muscles was high enough and lasted long enough to be an important mechanism in the lateral deviation of the head caused by unilateral labyrinthectomy.

Animals↗
PubMed1999

Evidence for a microglial reaction within the vestibular and cochlear nuclei following inner ear lesion in the rat.

Following unilateral inner ear lesion, astrocytes undergo hypertrophy in the deafferented vestibular and cochlear nuclei as shown by an increase in the level of glial fibrillary acid. The present study extends our understanding of vestibular and cochlear system plasticity by examining microglial changes in these deafferented nuclei. The microglial reaction was studied 1, 2, 4, 8, 14, 21, 28 and 42 days following the lesion with a monoclonal OX-42 antibody and lectins (Griffonia simplicifolia, B4 isolectin) labelled with horseradish peroxidase or fluorescein. The deafferented nuclei were also examined for apoptotic cells by terminal transferase-mediated nick end labelling of nuclear DNA fragments. In control and sham-operated rats, the distribution of the resting microglial cells was uniform in both the vestibular and cochlear nuclei. In the deafferented vestibular complex, the microglial cells increased in number, became hypertrophied and were distributed in the medial, lateral, superior and inferior vestibular nuclei. Reactive microglial cells were also detected in the ipsilateral cochlear nuclei. Some of the immunostained cells were hypertrophic whereas others presented an ameboid morphology with few short and stout processes. The microglial reaction was confined to the antero- and posteroventral cochlear nuclei. Finally, reactive microglia was also observed in the prepositus hypoglossi ipsilateral to the lesion. The microglial reactions within the prepositus hypoglossi, the vestibular and the cochlear nuclei were detectable as early as one day after the lesion and persisted several weeks in both the vestibular and cochlear nuclei. Apoptotic cells were not detected in the vestibular nuclei at any stage following the lesion. In contrast, terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were first detected in the deafferented cochlear nuclei on the 3rd day following the lesion. They reached an apparent maximum by day 8 and then declined until day 24. Double labelling experiments demonstrate that these cochlear terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were also lectin-positive suggesting that reactive cochlear lectin-positive microglia cells were eliminated by a programmed cell death. Our results establish the two experimental models as reliable tools to understand the role of microglia in adult brain plasticity. The cochlear microglial reaction was probably induced by the degeneration of the acoustic nerve which follows the acoustic ganglion destruction. Interestingly, the same reasoning cannot apply to the vestibular microglial reaction following unilateral labyrinthectomy: the vestibular ganglion was spared and the primary vestibular neurons did not degenerate, at least during the first week following the lesion.

Animals↗
PubMed1999

Saccular dysfunction in Meniere's disease.

OBJECTIVE: The aim of this study was to assess any dysfunction of the sacculus in patients with unilateral Meniere's disease by monitoring the vestibular evoked myogenic potentials (VEMPs) evoked by high level clicks on the Stemomastoid muscles (SCMs). STUDY DESIGN: The study was a retrospective analysis. SETTING: The study was performed in the E.N.T. department of the Lariboisière Hospital. PATIENTS: Fifty-nine patients aged 18 to 74 years with well-established unilateral Meniere's disease were included in the study. INTERVENTIONS: Loud monaural clicks were delivered unilaterally, and the VEMPs were recorded with skin electrodes on the ipsilateral SCM. All the patients were also subjected to a pure tone audiometric test and bithermal caloric testing. The postural performances of 39 patients were analyzed using the Equitest. MAIN OUTCOME MEASURE: VEMP results were the main outcome measure. RESULTS: The saccular response was absent on the affected side in 54% of the patients with Meniere's disease. This absence was correlated with the degree of low frequency hearing loss but not with canal paresis. Finally, nonfalling patients with saccular dysfunction had a significantly poorer postural performance than those without such dysfunction in the condition 5. CONCLUSION: Patients with Meniere's disease could have a saccular dysfunction (54% in this series). This saccular impairment correlated with low frequency hearing loss but not with canal paresis. Patients without VEMPs had poorer postural performances in condition 5 than those with normal VEMPs. Therefore, VEMP testing is useful for detecting patients at risk: in patients with saccular lesion, the dynamic postural performances should be assessed on a movable platform to detect visually dependent patients and to orient vestibular rehabilitation.

Adolescent↗
PubMed1998

Vestibular compensation revisited.

Vestibular compensation for the static and dynamic disorders induced by unilateral labyrinthectomy is a good model of plasticity in the central nervous system. After the lesion, the static deficits generally disappear in a few days, whereas recuperation of the dynamic, vestibular-related synergies is much slower and merely partial. The goal of this article is to reexamine some aspects of vestibular compensation in light of several recent findings. In the first part, we show that in vertebrates the organization of the neural networks underlying vestibular reflexes is deeply linked with the skeletal geometry of the animals. Accordingly, we propose that the neuronal mechanisms underlying vestibular compensation might be plane specific. We then deal with several issues related to the exact timing of vestibular compensation in various species. In the second part, we give several examples showing that vestibular compensation can now be studied at the molecular and cellular levels. For instance, we summarize some of our recent data, which indicate that glial cells could be strongly involved in the compensation process.

Adaptation, Physiological↗
PubMed1997

Dissociations between behavioural recovery and restoration of vestibular activity in the unilabyrinthectomized guinea-pig.

1. In the guinea-pig, a unilateral labyrinthectomy induces postural disturbances and an ocular nystagmus which abate or disappear over time. These behavioural changes are accompanied by an initial collapse and a subsequent restoration of the spontaneous activity in the neurones of the ipsilateral vestibular nuclei. Recently, it has been shown that the vestibular neuronal activity remained collapsed over at least 10 h whereas its restoration was complete 1 week after the lesion. The aims of this study were to determine when restoration of spontaneous activity in the partially deafferented vestibular neurones started and to compare the time courses of the behavioural and neuronal recoveries in guinea-pigs that had undergone a unilateral labyrinthectomy. 2. Neuronal discharge measurements were made using chronic extracellular recording of single unit activity. After a left labyrinthectomy, electrodes, were placed on the site of the destroyed labyrinth to enable stimulation of the left vestibular nerve. Behavioural measurements included chronic recording of eye movements by the scleral search coli technique. After a left labyrinthectomy, lateral deviation of the head, twisting of the head, and eye velocity of the slow phases of the nystagmus were measured. 3. The neuronal activity of the rostral part of the vestibular nuclear complex on the lesioned side was recorded in alert guinea-pigs over 4 h recording sessions between 12 and 72 h after the lesion. 4. The criterion used to select vestibular neurones for analysis was their recruitment by an electric shock on the vestibular nerve. In addition, in order to explore a uniform population, we focused on neurones recruited at monosynaptic latencies (0.85-1.15 ms). 5. For each recording period, the mean resting rate was calculated animal by animal and the grand mean of these individual resting rate means was calculated. Previously, a decline in the grand mean resting rate from 35.8 +/- 6.0 spikes s-1 (control state) to 7.1 +/- 4.2 spikes s-1 during the first 4 h after labyrinthectomy has been shown. In the present study, the first sign of recovery was observed during the 12-16 h recording period when the resting rate grand mean increased to 16.3 +/- 3.9 spikes s-1. This grand mean activity did not change significantly during the following 12 h. Thereafter, restoration of neuronal activity improved and was complete 1 week after the lesion. 6. Although the abatement of the vestibular symptoms roughly paralleled the restoration of neuronal activity in the vestibular nuclei, some discrepancies between the time courses of both phenomena emerged. An important step in postural recovery (the animals managed to stand up) and a major part of the abatement of the nystagmus occurred before the recovery of vestibular neuronal activity. In addition, lateral deviation of the head disappeared while restoration of the neuronal activity was incomplete, but significant head twisting was still evident when vestibular resting rates had recovered completely. 7. We conclude that restoration of neuronal activity in the ipsilateral vestibular nuclei starts 12 h after the lesion and that restoration of neuronal activity in the ipsilateral vestibular nuclei is not the only mechanism underlying behavioural vestibular compensation.

Animals↗