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P P Vidal

Publications and source records attributed to P P Vidal.

At least 19 recordsLinked to original sources
PubMed2003

Modulation of the voltage-gated sodium- and calcium-dependent potassium channels in rat vestibular and facial nuclei after unilateral labyrinthectomy and facial nerve transsection: an in situ hybridization study.

We investigated whether the expression in the vestibular and facial nuclei of the voltage-dependent Na alpha I and Na alpha III channels and of the Ca(2+)-activated K(+)-channel subunits, small-conductance (SK) 1, SK2 and SK3, is affected by unilateral inner-ear lesion including both labyrinthectomy and transsection of the facial nerve. Specific sodium (Na alpha I, Na alpha III) and potassium (SK1, SK2, SK3) radioactive oligonucleotides were used to probe sections of rat vestibular and facial nuclei by in situ hybridization methods. The signal was detected with films or by emulsion photography. Animals were killed at various times following the lesion: 1 day, 3 days, 8 days or 30 days. In normal adult animals, mRNAs for Na alpha I, and SK1, SK2, and SK3 channels were found in several brainstem regions including the lateral, medial, superior and inferior vestibular nuclei and the facial nuclei. In contrast, there was little Na alpha III subunit mRNA anywhere in the brainstem. Following unilateral inner ear lesion in rats, the medial vestibular nuclei were probed with Na alpha I, Na alpha III, SK1, SK2 and SK3 oligonucleotide probes: autoradiography indicated no difference between the two sides, at any of the times studied. Na alpha I and SK2 mRNAs were less abundant and Na alpha III, SK1 and SK3 mRNAs were more abundant in the axotomized facial nuclei motoneurons than in controls. Removal of vestibular input did not affect the abundance of the mRNAs for the sodium- or calcium-dependent potassium channels in the deafferented vestibular nuclei. There is thus no evidence that modulation of these conductances contributes to the recovery of a normal resting discharge of the deafferented vestibular neurons and consequently to the functional recovery of the postural and oculomotor deficits observed at the acute stage. However, facial axotomy induced a long-term modulation of both Na and SK conductances mRNAs in the facial motoneurons ipsilateral to the lesion. Presumably, retrograde injury factors resulting from axotomy were able to alter durably the membrane properties and thus the excitability of the facial motoneurons.

Animals↗
PubMed2002

Intratympanic gentamicin injections for Meniere disease: vestibular hair cell impairment and regeneration.

The authors treated 22 patients with intratympanic gentamicin. Vestibular function was measured using caloric and head impulse tests and vestibular evoked myogenic potentials induced by high amplitude sounds and short duration galvanic currents. Roughly one-third of the patients, after initially losing their caloric responses and displaying refixation saccades to head impulse tests, recovered within 2 years of the lesion. Vertigo did not recur in patients in whom the galvanic response was abolished.

Adult↗
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↗
PubMed2001

[Skeletal configurations of cervical column during rest to motion transition: generalization that underlie the motor repertoire in rodents].

During forward locomotion, guinea pigs adopted a posture which, although different, was as stereotyped as at rest. The whole extent of the vertebral column was extended, parallel to the earth-horizontal plane. This result supports the hypothesis that, in mammals, gaze and postural control by the central nervous system would be simplified by the adoption of a limited number of skeletal configurations. They would be optimized for energy saving, biomechanical efficacy and limitation of the number of degrees of freedom of the skeletal apparatus. Transition between rest and forward locomotion displayed two prominent characteristics: the head was stabilized versus space throughout the whole transition and the modifications of the skeletal geometry were confined to the median plane and to two major articular regions. Such an organization revealed a fourth characteristic of the guinea pig postural control: the skeletal configurations retained by evolution would ensure that smooth transitions take place between rest and the various activities of its motor repertoire. Finally, our purely descriptive data shed new light on the architecture of the neuronal network which underlies the vestibular control of gaze and posture.

Animals↗
PubMed2001

In vitro effects of acetyl-DL-leucine (tanganil) on central vestibular neurons and vestibulo-ocular networks of the guinea-pig.

For 40 years, the amino acid acetyl-DL-leucine (or isoleucine/Tanganil) has been used in clinical practice to reduce the imbalance and autonomic signs associated with acute vertigo crises. In animal models, acetyl-DL-leucine was shown to accelerate vestibular compensation following unilateral labyrinthectomy, while having only minor effects on normal vestibular function. However, the underlying mechanisms are unknown. In this study, the effect of acetyl-DL-leucine on the activity of central vestibular neurons of the medial vestibular nucleus (MVN) and/or the overall activity of vestibular-related networks was electrophysiologically measured in brainstem slices and in the isolated, in vitro whole brain (IWB) of guinea-pig. Only moderate effects were obtained in normal animals, where both excitatory and inhibitory actions of acetyl-DL-leucine were obtained. However, intracellular recordings from MVN neurons revealed that the nature of the response depended on the resting membrane potential. The neurons excited by acetyl-DL-leucine were significantly hyperpolarized compared to nonsensitive cells, whereas the neurons inhibited by this compound tended to display higher than normal membrane potentials. In accordance with these data, acetyl-DL-leucine reduced the prominent asymmetry characterizing the vestibular-related networks of IWBs taken from previously labyrinthectomized animals, by decreasing the activity of the abnormally depolarized neurons on the hyperactive side. Altogether, our results suggest that acetyl-DL-leucine might act mainly on abnormally hyperpolarized and/or depolarized MVN neurons, by bringing back their membrane potential towards a mean value of -65 to -60 mV. Since in animal models, acute vestibular disorders are associated with asymmetrical spontaneous activities of MVN neurons, this study suggests how acetyl-DL-leucine may reduce acute, vestibular-related imbalances in humans.

Abducens Nerve↗
PubMed2001

Modification of the pacemaker activity of vestibular neurons in brainstem slices during vestibular compensation in the guinea pig.

In the guinea pig, unilateral labyrinthectomy causes an immediate and severe depression of the spontaneous activity of the ipsilateral central vestibular neurons, which subsequently recovers completely within one week. A possible underlying mechanism could be an increase in the endogenous activity of the neurons deprived of their labyrinthine input. Here, we addressed this hypothesis. The endogenous activity of the neurons was assessed by their spontaneous activity recorded extracellularly in brainstem slices in the presence of a cocktail of neurotransmitter blockers (CNQX, D-APV, bicuculline and strychnine) which freed them from their main synaptic influences. The left medial vestibular nucleus (MVN) was explored in a very systematic way and strict methodological precautions were taken in order to validate comparisons between the numbers of spontaneously active neurons recorded in the MVN of distinct slices. In the presence of neurotransmitter antagonists, the mean number of spontaneously active neurons detected in a single MVN increased dramatically from 9.5 in slices from control guinea pigs to 26.3 in slices from animals labyrinthectomized on the left side one week beforehand. The mean firing rate of the recorded neurons also increased from 7.5 +/- 5.6 spikes/s in slices from control animals to 12.3 +/- 7.6 spikes/s in slices from guinea pigs labyrinthectomized one week beforehand. These results show that deprivation of the vestibular neurons of their labyrinthine input caused a change in the deprived neurons themselves. They suggest that an increase in pacemaker activity might be a factor responsible for the restoration of spontaneous activity in the vestibular neurons after labyrinthectomy.

2-Amino-5-phosphonovalerate↗
PubMed2001

Resonance of spike discharge modulation in neurons of the guinea pig medial vestibular nucleus.

The modulation of action potential discharge rates is an important aspect of neuronal information processing. In these experiments, we have attempted to determine how effectively spike discharge modulation reflects changes in the membrane potential in central vestibular neurons. We have measured how their spike discharge rate was modulated by various current inputs to obtain neuronal transfer functions. Differences in the modulation of spiking rates were observed between neurons with a single, prominent after hyperpolarization (AHP, type A neurons) and cells with more complex AHPs (type B neurons). The spike discharge modulation amplitudes increased with the frequency of the current stimulus, which was quantitatively described by a neuronal model that showed a resonance peak >10 Hz. Modeling of the resonance peak required two putative potassium conductances whose properties had to be markedly dependent on the level of the membrane potential. At low frequencies (< or =0.4 Hz), the gain or magnitude functions of type A and B discharge rates were similar relative to the current input. However, resting input resistances obtained from the ratio of the membrane potential and current were lower in type B compared with type A cells, presumably due to a higher level of active potassium conductances at rest. The lower input resistance of type B neurons was compensated by a twofold greater sensitivity of their firing rate to changes in membrane potential, which suggests that synaptic inputs on their dendritic processes would be more efficacious. This increased sensitivity is also reflected in a greater ability of type B neurons to synchronize with low-amplitude sinusoidal current inputs, and in addition, their responses to steep slope ramp stimulation are enhanced over the more linear behavior of type A neurons. This behavior suggests that the type B MVNn are moderately tuned active filters that promote high-frequency responses and that type A neurons are like low-pass filters that are well suited for the resting tonic activity of the vestibular system. However, the more sensitive and phasic type B neurons contribute to both low- and high-frequency control as well as signal detection and would amplify the contribution of both irregular and regular primary afferents at high frequencies.

Action Potentials↗
PubMed2000

Vestibular compensation modifies the sensitivity of vestibular neurones to inhibitory amino acids.

The progressive disappearance of the postural and oculomotor syndrome triggered by unilateral labyrinthectomy (vestibular compensation) is a model of plasticity in the adult central nervous system. This recovery may involve modifications of the pharmacological profile of central vestibular neurones, in particular their sensitivity to inhibitory amino acids. We therefore compared the sensitivity of medial vestibular nucleus neurones to glycine and muscimol in slices taken either from control animals, or from guinea-pigs labyrinthectomized 3 days before. We demonstrate that the loss of excitatory inputs experienced by the ipsilesional vestibular neurones induces a decrease in their sensitivity to inhibitory amino acids. These pharmacological changes should facilitate the recovery of a normal balance between the average resting discharge of neurones in both vestibular nuclei.

Adaptation, Physiological↗
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↗
PubMed2000

Floccular modulation of vestibuloocular pathways and cerebellum-related plasticity: An in vitro whole brain study.

The isolated whole brain (IWB) preparation of the guinea pig was used to investigate the floccular modulation of vestibular-evoked responses in abducens and oculomotor nerves and abducens nucleus; for identification of flocculus target neurons (FTNs) in the vestibular nuclei and intracellular study of some of their physiological properties; to search for possible flocculus-dependent plasticity at the FTN level by pairing of vestibular nerve and floccular stimulations; and to study the possibility of induction of long-term depression (LTD) in Purkinje cells by paired stimulation of the inferior olive and vestibular nerve. Stimulation of the flocculus had only effects on responses evoked from the ipsilateral (with respect to the stimulated flocculus) vestibular nerve. Floccular stimulation significantly inhibited the vestibular-evoked discharges in oculomotor nerves on both sides and the inhibitory field potential in the ipsilateral abducens nucleus while the excitatory responses in the contralateral abducens nerve and nucleus were free from such inhibition. Eleven second-order vestibular neurons were found to receive a short-latency monosynaptic inhibitory input from the flocculus and were thus characterized as FTNs. Monosynaptic inhibitory postsynaptic potentials from the flocculus were bicuculline sensitive, suggesting a GABA(A)-ergic transmission from Purkinje cells to FTNs. Two of recorded FTNs could be identified as vestibulospinal neurons by their antidromic activation from the cervical segments of the spinal cord. Several pairing paradigms were investigated in which stimulation of the flocculus could precede, coincide with, or follow the vestibular nerve stimulation. None of them led to long-term modification of responses in the abducens nucleus or oculomotor nerve evoked by activation of vestibular afferents. On the other hand, pairing of the inferior olive and vestibular nerve stimulation resulted in approximately a 30% reduction of excitatory postsynaptic potentials evoked in Purkinje cells by the vestibular nerve stimulation. This reduction was pairing-specific and lasted throughout the entire recording time of the neurons. Thus in the IWB preparation, we were able to induce a LTD in Purkinje cells, but we failed to detect traces of flocculus-dependent plasticity at the level of FTNs in vestibular nuclei. Although these data cannot rule out the possibility of synaptic modifications in FTNs and/or at other brain stem sites under different experimental conditions, they are in favor of the hypothesis that the LTD in the flocculus could be the essential mechanism of cellular plasticity in the vestibuloocular pathways.

Abducens Nerve↗
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

Intrinsic membrane properties and dynamics of medial vestibular neurons: a simulation.

The vestibulo-ocular and vestibulo-spinal network provides the ability to hold gaze fixed on an object during passive head movement. Within that network, most of the second-order neurons of the medial vestibular nucleus (MVNn) compute internal representations of head movement velocity in the horizontal plane. Our previous in vitro studies of the MVNn membrane properties indicated that they may play a major role in determining the dynamic properties of these neurons independently of their connectivity. The present study investigated that hypothesis at a theoretical level. Biophysical models of type A and B MVNn were developed. Two factors were found to be important in modeling tonic and phasic firing activity: the activation of the delayed potassium current and the rate of calcium flux. In addition, the model showed that the strength of the delayed potassium current may determine the different forms of action potentials observed experimentally. These two models (type A and B cells) were examined using depolarizing stimulation, random noise, step, ramp and sinusoidal inputs. For random noise, type A cells showed stable (regular) firing frequencies, while type B cells exhibited irregular activity. With step stimulation, the models exhibited tonic and phasic firing responses, respectively. Using ramp stimulations, frequency versus current curves showed a linear response for the type B neuron model. Finally, with sinusoidal stimulation of increasing frequencies, the type A model demonstrated a decrease in sensitivity, while the type B model exhibited an increase in sensitivity. These theoretical results support the hypothesis that MVNn intrinsic membrane properties specify various types of dynamic properties amongst these cells and therefore contribute to the wide range of dynamic responses which characterize the vestibulo-ocular and vestibulo-spinal network.

Action Potentials↗
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↗