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PubMed2006

Physiological and anatomical properties of mouse medial vestibular nucleus neurons projecting to the oculomotor nucleus.

Neurons in the medial vestibular nucleus (MVN) vary in their projection patterns, responses to head movement, and intrinsic firing properties. To establish whether neurons that participate in the vestibulo-ocular reflex (VOR) have distinct intrinsic physiological properties, oculomotor nucleus (OMN)-projecting neurons were identified in mouse brainstem slices by fluorescent retrograde labeling from the oculomotor complex and targeted for patch-clamp recordings. Such neurons were located in the magnocellular portion of the MVN contralateral to tracer injection, were mostly multipolar, and had soma diameters of around 20 mum. They fired spontaneous action potentials at rates higher than those of other MVN neurons and their spikes were of unusually short duration. OMN-projecting neurons responded to 1-s intracellular current injection with exceptionally high firing rates of >500 spikes/s. Their current-firing relationship was highly linear, with weak firing response adaptation during steady depolarization and little postinhibitory rebound firing after membrane hyperpolarization. Their firing responses were approximately in phase with sinusoidal current injection. The response dynamics of OMN-projecting neurons could be simulated with a simple integrate-and-fire model modified with the addition of small adaptation and rebound conductances. These findings indicate that the membrane properties of OMN-projecting neurons allow them to respond to head movements reliably and with high sensitivity but without substantially altering input dynamics.

Action Potentials↗
PubMed1978

Vestibular nucleus neurons relaying excitation from the anterior canal to the oculomotor nucleus.

A morphological approach was undertaken to determine which vestibular nucleus neurons relay excitation from the anterior canal to the IIIrd nucleus. In anesthetized rabbits HRP was iontophoresed into the IIIrd nucleus and cells filled with HRP reaction product (positive cells) searched for within the vestibular nuclear complex. By lesioning the MLF or brachium conjunctivum immediately after iontophoresis it was demonstrated that positive cells in the dorsum of the superior vestibular nucleus are backfilled via their axons which ascend in the brachium conjunctivum. By contrast positive cells in the center of the superior nucleus are backfilled via their axons in the MLF. In electrophysiological experiments in the presence of a severed MLF the anterior canal was selectively stimulated for orthodromic, and the 3rd nucleus stimulated for antidromic, activation of vestibular nucleus neurons. Recording extracellularly with glass microelectrodes filled with fast green FCF the only cells both ortho- and antidromically activated were localized to the dorsum of the superior vestibular nucleus. It is concluded that cells dorsally located in the superior nucleus relay the disynaptic excitatory vestibulo-ocular reflex from the anterior canal to the contralateral 3rd nucleus via their axons which ascend in the brachium conjunctivum.

Animals↗
PubMed1997

AMPA receptors in cultured vestibular ganglion neurons: detection and activation.

The presence and the activity of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) glutamate receptors were investigated in mouse cultured vestibular ganglion neurons using immunocytochemistry and measurement of intracellular calcium concentration ([Ca2+]i) by spectrofluorimetry. Cultures of dissociated vestibular ganglia from 18 gestation day mouse embryos were grown in vitro for 3-4 days. Immunocytochemical labelling of AMPA receptor subunits GluR2/R3 and GluR4 was detected in neuron cell bodies and proximal neurites and more lightly in glial cells. There was no clear selective subcellular localization of the different subunits. For the GluR1 subunit a signal was observed only in some neurons and neurites and was weak. Vestibular ganglion neurons responded to fast application of 1 mM glutamate and 10 mM aspartate through unknown receptors by a transient increase in [Ca2+]i. The mean amplitude of this rapid increase was about nine times the resting level and recovery was complete within 30-45 s after the application. If separated by an interval of at least 10 min, consecutive applications produced similar calcium responses. AMPA (1 mM) application induced the same type of responses. Five minutes prior to the AMPA exposure, the application of a specific AMPA antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1.5 mM), in the external medium inhibited the response to AMPA. Chelation of external calcium by EGTA (1.5 mM) abolished the responses to drug applications, indicating that an influx of external calcium is involved in the [Ca2+]i increase. These observations suggest that heteromeric AMPA receptors are expressed in vestibular ganglion neurons in culture and play a functional role in their glutamate-induced depolarization. Experiments are in progress using specific AMPA and NMDA antagonists to characterize the participation of the two types of ionotropic glutamate receptors in the glutamate/aspartate-induced intracellular calcium response.

Animals↗
PubMed1996

NMDA receptors of the vestibular nuclei neurones.

Cloning and pharmacological studies have shown that glutamatergic receptors can be divided in two classes (refer to Table 1): ionotropic receptors including N-methyl-D-aspartate (NMDA) and non-NMDA subtypes, and the G-protein-coupled metabotropic receptors (glutamate metabotropic receptor). There are two types of non-NMDA receptors: the AMPA/low-affinity kainate receptor type (the AMPA receptors) activated by a specific agonist, the alpha-amino-3-hydroxy-5-methyl-4-iso-xalone propionate (AMPA), and the high affinity kainate receptors. The vestibular nuclei neurones are endowed with all these types of glutamatergic receptors, which fits well with the fact that various afferents, including the primary vestibular afferents, most probably use glutamate or aspartate as a neurotransmitter. This article is aimed at summarising several past studies of our group and some more recent data obtained in the in vitro whole-brain preparation concerning the NMDA receptors of the central vestibular neurones. In that process, we will detail also many valuable studies of other groups that had been devoted to the same topic.

Animals↗
PubMed1987

Vestibular nuclear neuron activity during active and passive head movement in the alert rhesus monkey.

Responses of single neurons were recorded in the medial and descending vestibular nuclei (MVN and DVN) and in the deep cerebellar nuclei of three juvenile rhesus monkeys (Macaca mulatta). Neuronal activity was measured during both passive sinusoidal and nonsinusoidal whole body rotation (peak velocities were under 90 degrees/s) and during active head movements. Although the active head movements occasionally exceeded 300 degrees/s, most exhibited peak velocities of less than 200 degrees/s. A total of 133 units sensitive to horizontal head rotation were recorded, and of these, 38 were held for sufficient time to obtain both passive and active head movement data. Comparison of the neuronal firing patterns obtained during active and passive head movements revealed no apparent differences. Thus neurons that were observed to burst or pause during saccades with the head fixed continued to do so when the head was free. Both the sensitivity to head velocity and the "inferred" spontaneous firing rate were compared during active and passive head movements by plotting rate-velocity curves for both conditions. When the data points were fitted with linear regression lines, no statistically significant differences in either sensitivity or spontaneous rate were found. The present study provides no evidence that efferent vestibular activity alters the properties of afferent vestibular neurons during active head movements, as has previously been suggested (21). Furthermore, neurons in the rostral portions of the vestibular nuclei in primates encode head velocity based entirely on labyrinthine information. Neither neck proprioceptors nor an efference copy of the head movement motor program seem to contribute significantly to the firing patterns observed.

Animals↗
PubMed1999

Lesion-induced plasticity in rat vestibular nucleus neurones dependent on glucocorticoid receptor activation.

1. We have recently shown that neurones in the rostral region of the medial vestibular nucleus (MVN) develop a sustained increase in their intrinsic excitability within 4 h of a lesion of the vestibular receptors of the ipsilateral inner ear. This increased excitability may be important in the rapid recovery of resting activity in these neurones during 'vestibular compensation', the behavioural recovery that follows unilateral vestibular deafferentation. In this study we investigated the role of the acute stress that normally accompanies the symptoms of unilateral labyrinthectomy (UL), and in particular the role of glucocorticoid receptors (GRs), in the development of the increase in excitability in the rostral MVN cells after UL in the rat. 2. The compensatory increase in intrinsic excitability (CIE) of MVN neurones failed to occur in animals that were labyrinthectomized under urethane anaesthesia and kept at a stable level of anaesthesia for either 4 or 6 h after UL, so that they did not experience the stress normally associated with the vestibular deafferentation syndrome. In these animals, 'mimicking' the stress response by administration of the synthetic GR agonist dexamethasone at the time of UL, restored and somewhat potentiated CIE in the MVN cells. Administration of dexamethasone in itself had no effect on the intrinsic excitability of MVN cells in sham-operated animals. 3. In animals that awoke after labyrinthectomy, and which therefore experienced the full range of oculomotor and postural symptoms of UL, there was a high level of Fos-like immunoreactivity in the paraventricular nucleus of the hypothalamus over 1.5-3 h post-UL, indicating a strong activation of the stress axis. 4. The GR antagonist RU38486 administered at the time of UL abolished CIE in the rostral MVN cells, and significantly delayed behavioural recovery as indicated by the persistence of circular walking. The mineralocorticoid receptor (MR) antagonist spironolactone administered at the time of UL had no effect. 5. Vestibular compensation thus involves a novel form of 'metaplasticity' in the adult brain, in which the increase in intrinsic excitability of rostral MVN cells and the initial behavioural recovery are dependent both on the vestibular deafferentation and on the activation of glucocorticoid receptors, during the acute behavioural stress response that follows UL. These findings help elucidate the beneficial effects of neuroactive steroids on vestibular plasticity in various species including man, while the lack of such an effect in the guinea-pig may be due to the significant differences in the physiology of the stress axis in that species.

Anesthesia↗
PubMed1982

Canal-neck interaction in vestibular nuclear neurons of the cat.

The convergence and interaction of horizontal semicircular canal and neck proprioceptive inputs were studied in neurons of the caudal two thirds of the vestibular nuclear complex. Extracellular neuron activity was recorded under muscle relaxation and slight anesthesia in chronically prepared cats. The following stimulations were applied: horizontal rotations of (a) the whole body (labyrinth stimulation), (b) the trunk vs. the stationary head (neck stimulation), and (c) the head vs. the stationary trunk (combined labyrinth and neck stimulation). Of 152 neurons investigated, 83 (55%) showed convergence of the two inputs. In about half of these neurons, the neck input was very weak and hardly affected the labyrinthine response during head rotation. Judged from the response pattern, several of these neurons presumably were related to vestibulo-oculomotor function (i.e., vestibular nystagmus). In the other half (i.e., 27% of all neurons), sensitivity of the two inputs was similar. Both labyrinthine and neck responses contained a dynamic ("velocity") component; neck responses of more than half of these neurons had, in addition, a static ("position") component. The dynamic components were either "antagonistic" or "synergistic" as to their convergence during head rotation. When applying this combined stimulation, the dynamic components summed linearly, yielding subtration in case of antagonistic convergence and addition in case of synergistic convergence. In contrast, the static components of the neck responses remained largely unchanged during head rotation. However, the static head-to-trunk deflection determined the tonic discharge level in such neurons and thus facilitated or disfacilitated the dynamic responses to superimposed labyrinth stimulation. We suggest that the two patterns of labyrinthine neck interaction observed in vestibular nuclear neurons, i.e., subtration and addition, may be involved in the postural control of the trunk and head, respectively. In contrast, interference of the neck input with vestibulo-oculomotor function appears to be almost negligible in the intact cat.

Animals↗
PubMed1999

The ultrastructure of GABA-immunoreactive vestibular commissural neurons related to velocity storage in the monkey.

The purpose of the present study was to visualize the synaptic interactions of GABAergic neurons involved in the mediation of velocity storage. In the previous report, ultrastructural studies of degenerating neurons were conducted following midline section of rostral medullary commissural fibers with subsequent behavioral testing. The midline lesion caused functionally discrete damage to the velocity storage component, but not to the direct pathway, of the angular vestibulo-ocular reflex, and the degenerating neurons were interpreted as potential participants in the velocity storage network. We concluded that at least some of the commissural axons mediating velocity storage originate from clusters of neurons in the lateral crescents of the rostral medial vestibular nucleus. In the present report, immunocytochemical evidence is presented that many vestibular commissural neurons, putatively involved in mediating velocity storage, are GABAergic. These cells have large nuclei, small round or narrow tubular mitochondria, occasional cisterns and vacuoles, but few other organelles. Their axons are thinly-myelinated, and terminate in boutons containing mitochondria of similar ultrastructural appearance and a moderate density of round/pleomorphic synaptic vesicles. Such terminals often form axoaxonic synapses, and less frequently axodendritic contacts, with non-GABAergic elements. On the basis of the present results, we conclude that a portion of the commissural neurons of the velocity storage pathway is GABAergic. The observation of GABAergic axoaxonic synapses in this pathway is interpreted as a structural basis for presynaptic inhibition of medial vestibular nucleus circuits by velocity storage-related commissural neurons. Conversely, substantial ultrastructural evidence for postsynaptic inhibition of non-GABAergic commissural cells argues for a dual role for GABAergic terminals mediating velocity storage: presynaptic inhibition of non-GABAergic vestibular cells by GABAergic velocity storage commissural axons, and postsynaptic inhibition of non-GABAergic velocity storage cells by GABAergic axons. Both pre- and postsynaptic inhibitory arrangements could provide the morphologic basis for disinhibitory activation of the velocity storage network within local neuronal circuits.

Animals↗
PubMed1977

Time constants of vestibular nuclei neurons in the goldfish: a model with ocular propioception.

A simple model of the vestibular-ocular reflex with a proprioceptive eye velocity feedback loop is used to simulate recent data on the vestibular responses of neurons in the vestibular nuclei of spinal goldfish. The data support the hypothesis that a proprioceptive feedback loop elongates the vestibular nucleus time constant to equal that of the slow phase eye movements of vestibular nystagmus.

Animals↗
PubMed1976

Electron microscopic investigation of the vestibular projection to the cat trochlear nuclei.

Ultrastructural degeneration studies were carried out on the cat trochlear nucleus following lesion of the vestibulo-trochlear pathway in order to characterize the location and type of presynaptic endings involved in this pathway. Four types of boutons are found in the normal trochlear nucleus. Types I and II are large and demonstrate typical en passant profiles with small diameter synaptic vesicles (35 and 40 nm). These terminals are characterized by the absence of neurofilaments in the Type II endings. Types III and IV are smaller boutons, located more axondendritically, and contain larger diameter synaptic vesicles (45 nm). Type V terminals contain large, granulated vesicles and occur only rarely. Following the interruption of the ascending projection from the ipsilateral superior and medial vestibular nuclei by parasagittal medullary lesions, degeneration of Type II boutons was commonly encountered in the ipsilateral trochlear nucleus. Predominantly Type III degeneration was found in the contralateral trochlear nucleus. Electrical stimulation of the vestibular nerve showed that these lesions resulted in (1) a complete loss of inhibition in the ipsilateral trochlear nucleus and (2) a significant (75-90%) reduction in the contralateral excitatory pathway to the trochlear nucleus. Midline sagittal lesions in the floor of the fourth ventricle interrupting the decussating fiber projection from the bilateral medial vestibular nuclei resulted in selective degeneration of only Type III boutons in both trochlear nuclei. We conclude that inhibitory vestibular neurons eminating from the superior vestibular nucleus terminate on trochlear motoneurons with Type II boutons and excitatory vestibular neurons from the contralateral medial vestibular nucleus end on trochlear motoneurons with Type III boutons.

Animals↗
PubMed1999

Integration of vestibular and head movement signals in the vestibular nuclei during whole-body rotation.

Single-unit recordings were obtained from 107 horizontal semicircular canal-related central vestibular neurons in three alert squirrel monkeys during passive sinusoidal whole-body rotation (WBR) while the head was free to move in the yaw plane (2.3 Hz, 20 degrees /s). Most of the units were identified as secondary vestibular neurons by electrical stimulation of the ipsilateral vestibular nerve (61/80 tested). Both non-eye-movement (n = 52) and eye-movement-related (n = 55) units were studied. Unit responses recorded when the head was free to move were compared with responses recorded when the head was restrained from moving. WBR in the absence of a visual target evoked a compensatory vestibulocollic reflex (VCR) that effectively reduced the head velocity in space by an average of 33 +/- 14%. In 73 units, the compensatory head movements were sufficiently large to permit the effect of the VCR on vestibular signal processing to be assessed quantitatively. The VCR affected the rotational responses of different vestibular neurons in different ways. Approximately one-half of the units (34/73, 47%) had responses that decreased as head velocity decreased. However, the responses of many other units (24/73) showed little change. These cells had signals that were better correlated with trunk velocity than with head velocity. The remaining units had responses that were significantly larger (15/73, 21%) when the VCR produced a decrease in head velocity. Eye-movement-related units tended to have rotational responses that were correlated with head velocity. On the other hand, non-eye-movement units tended to have rotational responses that were better correlated with trunk velocity. We conclude that sensory vestibular signals are transformed from head-in-space coordinates to trunk-in-space coordinates on many secondary vestibular neurons in the vestibular nuclei by the addition of inputs related to head rotation on the trunk. This coordinate transformation is presumably important for controlling postural reflexes and constructing a central percept of body orientation and movement in space.

Animals↗
PubMed1991

Role of premotor vestibular nucleus neurons in vertical gaze.

The firing properties and projection patterns of secondary vestibular nucleus neurons involved in the vertical vestibulo-ocular pathways were investigated in alert cats. Recordings were made in the medial longitudinal fasciculus (MLF) from axons that were monosynaptically activated from the vestibular nerve. Many identified axons discharged in relation to vertical eye movements. The majority of these axons increased their firing rate for downward eye position (DPVs). During pitch rotation, the firing rate of DPVs was also related to upward head velocity, suggesting that they received monosynaptic input from the posterior canal. DPVs could be divided into two groups on the basis of their firing regularity. There was a tendency for regular DPVs to have a higher firing rate, a higher correlation for the rate-position relationship, and a larger phase lag and a smaller gain re head velocity than irregular DPVs. Spike-triggered average method and intraaxonal HRP techniques demonstrated that ipsilaterally projecting (i-) DPVs made inhibitory connections with up-on extraocular motoneurons, and contralaterally projecting (c-) DPVs made excitatory connections with down-on motoneurons. Virtually all i-DPVs were of regular type, while c-DPVs included both regular and irregular types. Stimulation of the caudal MLF at the level of the obex indicated that all the irregular c-DVPs and some of the regular c-DPVs had a collateral to the spinal cord, while none of the regular i-DPVs had such a collateral.

Animals↗
PubMed2002

Regulation of firing response gain by calcium-dependent mechanisms in vestibular nucleus neurons.

Behavioral reflexes can be modified by experience via mechanisms that are largely unknown. Within the circuitry for the vestibuloocular reflex (VOR), neurons in the medial vestibular nucleus (MVN) show adaptive changes in firing rate responses that are correlated with VOR gain (the ratio of evoked eye velocity to input head velocity). Although changes in synaptic strength are typically assumed to underlie gain changes in the VOR, modulation of intrinsic ion channels that dictate firing could also play a role. Little is known, however, about how ion channel function or regulation contributes to firing responses in MVN neurons. This study examined contributions of calcium-dependent currents to firing responses in MVN neurons recorded with whole cell patch electrodes in rodent brain stem slices. Firing responses were remarkably linear over a wide range of firing rates and showed modest spike frequency adaptation. Firing response gain, the ratio of evoked firing rate to input current, was reduced by increasing extracellular calcium and increased either by lowering extracellular calcium or with antagonists to SK- and BK-type calcium-dependent potassium channels and N- and T-type calcium channels. Blockade of SK channels occluded gain increases via N-type calcium channels, while blocking BK channels occluded gain increases via presumed T-type calcium channels, indicating specific coupling of potassium channels and their calcium sources. Selective inhibition of Ca(2+)/calmodulin-dependent kinase II and broad-spectrum inhibition of phosphatases modulated gain via BK-dependent pathways, indicating that firing responses are tightly regulated. Modulation of firing response gain by phosphorylation provides an attractive mechanism for adaptive control of VOR gain.

Amiloride↗
PubMed1987

Inputs from regularly and irregularly discharging vestibular nerve afferents to secondary neurons in the vestibular nuclei of the squirrel monkey. I. An electrophysiological analysis.

1. The electrical excitability of vestibular nerve afferents is related to their discharge regularity (23). Irregular (I) afferents are more excitable than regular (R) afferents. We explored the possibility that the differences in electrical excitability could be used to determine the profile of monosynaptic inputs from the ipsilateral vestibular nerve (Vi) to secondary neurons of the vestibular nuclei. The growth of monosynaptic Vi excitatory postsynaptic potentials (EPSPs) as shock strength is increased should reflect the kinds of afferent input that a secondary neuron receives. We were particularly interested in seeing if cells in the vestibular nuclei could be distinguished as R or I neurons depending on whether they received predominantly regular or irregular inputs. Barbiturate-anesthetized squirrel monkeys were used. 2. Recordings were made from vestibular nerve afferents. Shock strength was expressed as multiples of T, the value needed to recruit 10% of the afferents or, as determined empirically, to evoke a detectable field potential in the vestibular nuclei. Most I afferents (85/87 = 98%) were recruited below 4 X T, whereas most R afferents (197/212 = 93%) were first activated above 4 X T. The relation between latent period and electrical excitability was flat for units with thresholds in the range 1-4 X T. Latent periods increased for units with higher thresholds, especially those first activated above 8 x T. The threshold differences between I and R afferents are maximal if the shock falls at approximately half the mean interval after a naturally occurring action potential. The same results were obtained by having each unit fire to a maximal (16-32 X T) conditioning shock and then determining the threshold to a test shock presented 4 ms later. The latter stimulus configuration was used to study the Vi monosynaptic inputs to secondary neurons. The test shock was raised by successive doublings from 1 X T to the strength of the conditioning shock (16-32 X T). 3. Intracellular recordings were made from neurons located in the superior vestibular nucleus or the rostral parts of the medical or lateral vestibular nuclei. Amplitudes and latent periods of Vi EPSPs were measured from averages of several repetitions of each stimulus pair. Each EPSP was calculated by subtracting the extracellular from the intracellular averaged response. Of the 122 neurons sampled, 115 were judged to be monosynaptically related to the ipsilateral vestibular nerve because their Vi EPSPs had latent periods in the range of 0.7-1.4 ms.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1980

Selective effect of ethanol on the vestibular nucleus neurons in the cat.

Effects of intravenous administration of ethanol on the neuronal activities of the lateral vestibular nucleus (LVN) and spinal trigeminal nucleus (STN) were investigated in cats. The LVN neurons were classified into three groups according to the latency of the first spike elicited by orthodromic vestibular nerve stimulation and antidromic vestibulospinal tract stimulation: monosynaptic, polysynaptic I and polysynaptic II neurons. Ethanol of 0.2--1.6 g/kg dose-dependently suppressed the orthodromic spike generation of the monosynaptic and polysynaptic II neurons without affecting their latency and antidromic spike generation of the former neuron. The mean spike numbers of the monosynaptic and polysynaptic II neurons were significantly decreased with ethanol over 0.4 g/kg. The polysynaptic I neuron, however, remained unaffected by the drug up to 0.8 g/kg. Similarly, the spike generation of the STN relay neuron and interneuron elicited by trigeminal nerve stimulation remained unaltered with ethanol given in doses up to 0.8 g/kg. These results indicate that small doses of ethanol more selectively interfere with synaptic transmission in the LVN monosynaptic and polysynaptic II neurons than transmission in the STN relay neurons and interneurons.

Action Potentials↗
PubMed1981

Vestibular efferent neurons and catecholamine cell groups in the reticular formation of the pigeon.

This study was designed to investigate the relationship between vestibular efferent neurons and catecholamine cell groups within the reticular formation of the pigeon. Horseradish peroxidase (HRP) was injected into the endolymphatic space of one labyrinth. The brain was perfused with glyoxylic acid and serial sections were examined with a fluorescence microscope. After documentation of the location of fluorescent cells the sections were reacted for HRP with tetramethylbenzidine. Fluorescent cells were noted intermingled among the HRP-labeled vestibular efferent neurons in the nucleus reticularis pontis caudalis. No neurons were both fluorescent and HRP-positive. Fluorescent cells were also noted bilaterally in locus ceruleus, raphe nucleus, and in close proximity to the abducent, facial, hypoglossal and ambiguus nuclei.

Animals↗
PubMed1978

Selective effect of cinnarizine on the vestibular nucleus neurons.

Effects of cinnarizine were studied on the lateral vestibular nucleus (LVN) and spinal trigeminal nucleus (STN) of cats anesthetized with alpha-chloralose. Cinnarizine did not produce any obvious alterations of the field potential and spike generation of type B interneurons in STN elicited by trigeminal nerve stimulation as well as the field potential in LVN by vestibular nerve stimulation. Spike generation of monosynaptic LVN neurons elicited by the suprathreshold stimulus to the vestibular nerve was unaffected by cinnarizine up to 4 mg/kg. When the subthreshold stimulus was applied to the vestibular nerve, however, the spike number of LVN monosynaptic neurons was significantly increased after cinnarizine treatment. The enhancement of spike firing by cinnarizine upon both supra- and subthreshold stimuli to the vestibular nerve was found to be more pronounced in LVN polysynaptic neurons than monosynaptic ones. Since the effect of cinnarizine on LVN neurons was not dose-dependent, it is suggested that the enhanced responsiveness of the neurons by the drug might be due to an increase of blood flow, but not to a direct excitation of the neurons themselves.

Animals↗
PubMed1993

Morphological correlations between spontaneously discharging primary vestibular afferents and vestibular nucleus neurons in the cat.

Synaptic connections between physiologically classified primary vestibular afferents (PVAs) and their target vestibular nucleus (VN) neurons were examined by a combination of intra-axonal staining and electron microscopic techniques. PVAs originating from the horizontal semicircular canal were electrophysiologically classified as either regular- or irregular-type based on the regularity of their spontaneous discharge patterns, and were intra-axonally labeled with horseradish peroxidase (HRP). HRP-labeled PVAs of both types had many swellings along their course that contacted VN neurons. These swellings contained spherical synaptic vesicles and showed asymmetric postsynaptic specialization. Target VN neurons of both types of PVAs were distributed primarily in the superior, medial, and inferior VN. Irregular-type PVAs made more axosomatic contacts than did regular-type PVAs. The soma size of target VN neurons and the number of terminal boutons per target VN neuron were larger for irregular-type PVAs than for regular-type PVAs. Large VN neurons (presumably kinetic neurons) were innervated exclusively by irregular-type PVAs. Small VN neurons were innervated by PVAs of the regular-type and the irregular-type. These results demonstrate that there is a correlation between the physiological properties and morphological characteristics of PVAs and their target VN neurons.

Animals↗