Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vestibular Neuronitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1997

[Effects of acetyl-DL-leucine on the recovery of the locomotor equilibrium and spontaneous discharge of lateral vestibular nucleus neurons in unilateral vestibular neurectomized cats].

The effects of acetyl-DL-leucine (AL) treatment (28 mg/kg.day, p.o.) on the vestibular compensation were studied over period of 6 weeks in unilateral vestibular neurectomized cats. This investigation was performed by measuring the recovery time of locomotor equilibrium in the rotating beam test and recording the unitary extracellular activity of single neurons of lateral vestibular nucleus (LVN) in totally awake cats. The results showed that AL treatment strongly accelerated the recovery of locomotor equilibrium and significantly inhibited the recovery of resting spontaneous firing rate within the deafferented LVN neurons (n = 506) but improved the sensitivity and recovery of relative amount and proportion of neurons (n = 454) in response to head roll tilts in frontal plane. The neurophysiological mechanisms of AL role in the vestibular compensation were discussed.

Animals↗
PubMed1986

Effects of lesion of the interstitial nucleus of Cajal on vestibular nuclear neurons activated by vertical vestibular stimulation.

Experiments were performed in cats anesthetized with nitrous oxide to study the effects of INC lesions on responses of vestibular nuclear neurons during sinusoidal rotations of the head in the vertical (pitch) plane. Responses of neurons in the INC region were recorded during pitch rotations at 0.15 Hz. A great majority of these neurons did not respond to static pitch tilts, and they seemed to respond either to anterior or to posterior semicircular canal inputs with a peak phase lag of 140 deg (re head acceleration). Responses of vestibular nuclei neurons in intact cats were recorded during pitch rotations at the same frequency (0.15 Hz). Neurons that seemed to respond to vertical semicircular canal inputs showed peak phase lags of 90 deg relative to head acceleration, whereas neurons that responded to static pitch tilts showed peak phase shifts near 0 deg. These results indicate that responses of neurons in the INC region lag those of vestibular neurons by about 50 deg, suggesting that the former neurons possess a phase-lagging (i.e. integrated) vestibular signal. Responses of vestibular neurons in cats that had received electrolytic lesions of bilateral INCs 1-2 weeks previously were recorded during pitch rotations at the same frequency (0.15 Hz). Neurons that presumably responded to vertical semicircular canal inputs showed a peak phase lag of 60 deg relative to head acceleration, a significant decrease of the phase lag compared to normal, whereas responses near 0 deg were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Firing characteristics of vestibular nuclei neurons in the alert monkey after bilateral vestibular neurectomy.

After destruction of the peripheral vestibular system which is not activated by moving large-field visual stimulation, not only labyrinthine-ocular reflexes but also optokinetic-ocular responses related to the "velocity storage" mechanism are abolished. In the normal monkey optokinetic-ocular responses are reflected in sustained activity changes of central vestibular neurons within the vestibular nuclei. To account for the loss of optokinetic responses after labyrinthectomy, inactivation of central vestibular neurons consequent on the loss of primary vestibular activity is assumed to be of major importance. To test this hypothesis we recorded the neural activity within the vestibular nuclear complex in two chronically prepared Rhesus monkeys during a period from one up to 9 and 12 months after both vestibular nerves had been cut. The discharge characteristics of 829 cells were studied in relation to eye fixation, and to a moving small and large (optokinetic) visual stimulus producing smooth pursuit (SP) eye movements and optokinetic nystagmus (OKN). Units were grouped into different subclasses. After chronic bilateral vestibular neurectomy (BVN) we have found: (1) a rich variety of spontaneously active cells within the vestibular nuclear complex, which--as far as comparison before and after BVN is possible--belong to all subclasses of neurons functionally defined in normal monkey; and (2) no sustained activity changes which are related to the activation of the "velocity storage" mechanism; this is especially true for "pure-vestibular", "vestibular-pause" and "tonic-vestibular-pause" cells in normal monkey which show a "pure", "pause" and "tonic-pause" firing pattern after BVN. Neurons which are modulated by eye position are, however, modulated with the velocity of slow eye movements with comparable sensitivity during SP and OKN. Retinal slip is extremely rarely encoded. The results of the present study do not directly answer the question why the "velocity storage" mechanism is abolished after BVN but they suggest that only a small number of central vestibular cells may be inactivated by neurectomy.

Animals↗
PubMed1984

Mode of synaptic transmission between vestibular afferents and neurons of the vestibular nucleus in the frog.

Excitatory postsynaptic potentials (EPSPs) were evoked in vestibular neurons of the isolated frog brainstem by stimulation of the ipsilateral vestibular nerve or by direct intra-axonal activation of single vestibular fibers. Composite as well as single-fiber EPSPs usually displayed two components. A Ca2+-deficient, Mn2+-containing solution abolished the delayed chemical components of the EPSPs, but did not affect the short latency responses suggesting a dual (electrical-chemical) mode of transmission between some vestibular afferents and vestibular neurons.

Afferent Pathways↗
PubMed2002

The contribution of the intrinsic excitability of vestibular nucleus neurons to recovery from vestibular damage.

Damage to the peripheral vestibular system results in a syndrome of ocular motor and postural abnormalities that partially and gradually abate over time in a process known as 'vestibular compensation'. The first, rapid, phase of compensation has been associated with a recovery of spontaneous resting activity in the ipsilateral vestibular nucleus complex (VNC), as a consequence of neuronal and synaptic plasticity. Increasing evidence suggests that normal VNC neurons in labyrinthine-intact animals, as well as ipsilateral VNC neurons following unilateral vestibular deafferentation (UVD), rely to some extent on intrinsic pacemaker activity provided by voltage-dependent conductances for their resting activity. Modification of this intrinsic pacemaker activity may underlie the recovery of resting activity that occurs in ipsilateral VNC neurons following UVD. This review summarizes and critically evaluates the 'intrinsic mechanism hypothesis', identifying discrepancies amongst the current evidence and suggesting experiments that may test it further.

Action Potentials↗
PubMed1990

Inhibition by intravenously administered sodium bicarbonate of neuronal activity in medial vestibular nucleus neurons.

The effects of 7% sodium bicarbonate on medial vestibular nucleus (MVN) neurons were examined to elucidate the mechanism underlying its anti-vertigo action, using alpha-chloralose-anesthetized cats. Intravenous injection of the drug at 1, 2 and 4 ml/kg every 10 min dose-dependently inhibited rotation- and glutamate-induced firing of type 1 neurons, although a low dose of the drug enhanced firing in a few neurons. However, microiontophoretic application of bicarbonate ions did not inhibit rotation- or glutamate-induced firing. After injection of the drug, the Po2 level in arterial blood did not differ from previous levels, but the bicarbonate ion levels dose-dependently increased concomitantly with an increase in pH, as compared with previous levels. These results suggest that the intravenous injection of 7% sodium bicarbonate directly inhibits the neuronal activity of the MVN, although the lower dose may enhance neuronal activity by acting on the peripheral vestibule.

Animals↗
PubMed1993

Different calcium-binding proteins identify subpopulations of vestibular ganglion neurons in the rat.

Vestibular neurons were studied by cytochrome oxidase (CO) histochemistry and by immunocytochemistry using antibodies against parvalbumin (PV), calbindin (CaBP), calretinin (CaR) and 160 KD neurofilament protein (NF). All the neurons present a high level of CO activity and a high content of PV. CaBP and CaR are restricted to a specific population of about 16% of the neurons and are among the largest ones. The latter neurons also have a high density of NF 160 KD protein. In conclusion the biochemical characteristics of the vestibular ganglion neurons are discussed in relation to their morphological and physiological properties.

Animals↗
PubMed1991

Ultrastructural evidence that early synapse formation on central vestibular sensory neurons is independent of peripheral vestibular influences.

Migration and early differentiation of neurons of the tangential vestibular nucleus of the chick take place between embryonic days 5 and 8. In the absence of primary vestibular afferents (otocyst-ablation), a previous light microscope study documented that early developmental events still occurred, but the neurons failed to complete differentiation and to survive. In order to understand why these neurons undergo normal early development, we have repeated the vestibular deafferentation paradigm followed by ultrastructural observations on these neurons. We found that the ultrastructural events associated with migration and differentiation in the deafferented tangential nucleus were essentially normal from 5 to 8 days. Most important, longitudinal fibers, presumably of central, nonvestibular origins, formed the first synapses at the same time and sequence as observed in normal embryos. Thus vestibular sensory neurons receive their first input from central fibers, initiating events in the formation of a central vestibular circuitry without the influence of peripheral vestibular fibers or endorgan.

Animals↗
PubMed1975

Effects of chlorpromazine and diazepam on neuronal activities of the lateral vestibular nucleus in cats.

The effects of chlorpromazine and diazepam on vestibular neuronal activity were studied in gallamine immobilized cats. Chlorpromazine depressed all the P, N1 and N2-waves of field potentials in the lateral vestibular nucleus evoked by electrical stimulation of the vestibular nerve. Diazepam also reduced the amplitude of postsynaptic components (N1 and N2-waves), while the presynaptic one (P-wave) was slightly increased. Chlorpromazine suppressed the spontaneous as well as the increased vestibular neuronal firing following stimulation of the vestibular nerve. Diazepam enhanced the increased vestibular neuronal firing excited by the nerve stimulation and had no effect on the spontaneous unitary discharges.

Animals↗
PubMed2001

Adult rat otic placode-derived neurons and sensory epithelium express all four erbB receptors: a role in regulating vestibular ganglion neuron viability.

The erbB receptor family consists of erbB1/epidermal growth factor receptor, erbB2/neu, erbB3, and erbB4, all of which have been implicated in cell proliferation, differentiation, and survival in several tissues. In the nervous system, these family members can function in a trophic capacity for certain subpopulations of neurons and some types of non-neuronal cells. Vestibular sensory epithelial cells and vestibular ganglion neurons are derived from ectodermal otic placode and are essential components of the peripheral vestibular system, the sensory system for balance. Recent studies in mammals suggest that certain ligands of the epidermal growth factor receptor can induce proliferation of vestibular sensory epithelial cells. We now show that vestibular ganglion neurons and vestibular sensory epithelial cells express all four erbB receptors in adult rats. Cultured vestibular ganglion neurons also expressed all four erbB family members and were therefore used to analyze the effects of modulating erbB signaling on differentiated vestibular ganglion neurons. Transforming growth factor-alpha (a ligand for epidermal growth factor receptor) and sensory and motor neuron-derived factor (a ligand for erbB3 and erbB4) promoted vestibular ganglion neuron viability, whereas epidermal growth factor (another ligand for epidermal growth factor receptor) did not. Glial growth factor 2 (another ligand for erbB3 and erbB4) and an antibody that blocks erbB2/neu-mediated signaling inhibited vestibular ganglion neuron viability. Collectively, these observations indicate that erbB signaling regulates the viability of differentiated otic placode-derived cells in mammals and suggest that exogenous modulation of erbB signaling in peripheral vestibular tissues may prove therapeutically useful in peripheral vestibular disorders.

Animals↗
PubMed1978

Transfer characteristics of neurons in vestibular nuclei of the alert monkey.

1. In the alert monkey, 74 neurons in the vestibular nuclei were investigated during sinusoidal rotation about a vertical axis at frequencies between 0.003 and 0.5 Hz. Phase and gain were determined by a fast Fourier analysis program. 2. Phase advance, relative to turntable velocity, was small between 0.05 and 0.5 Hz. At lower frequencies phase advance increased to 45 degrees at 0.007--0.02 Hz, and 90 degrees at 0.003--0.005 Hz. In agreement with the phase characteristics, a gain decrease of -3 dB was determined between 0.007 and 0.02 Hz. Assuming a linear system, time constants of 9.5, 11.9, and 24.5 s were calculated for three different monkeys. 3. Simultaneously recorded nystagmus exhibited similar time constants as the central vestibular neurons for each monkey. 4. Frequency responses of 11 neurons were recorded from the same monkeys while they were under general anesthesia and the time constants were reduced to 4--7 s. This is the range of time constants seen in the peripheral nerve. 5. The longer time constants in the alert state are due to an integration process, which provides a low-frequency compensation, and is thought to be achieved through a feedback loop involving the reticular formation. 6. In the alert and anesthetized state, monkeys were also exposed to velocity trapezoids. Time constants of decay of neuronal activity were in good agreement with the data obtained during sinusoidal stimulation. 7. A transfer function of the primary vestibular afferents is expanded to include the described low-frequency compensation found in central vestibular neurons in the alert animals.

Anesthesia, General↗
PubMed2001

Isolated vestibular areflexia after blunt head trauma.

The sudden unilateral loss of vestibular function is a frequent cause of vertigo. This condition is called vestibular neuronitis or vestibular neuritis. Its cause remains unknown, but many authors consider it to be a sequel of vestibular viral infection. We report the history and clinical findings of 5 patients in whom a unilateral vestibular loss occurred after head trauma. None of these patients complained of hearing loss. In all cases, the vertigo gradually subsided over days or weeks. The follow-up showed the partial recovery of vestibular function in 2 cases, while vestibular areflexia persisted in 3. The clinical course and findings were similar in every respect to those in patients with classic idiopathic vestibular neuronitis.

Adult↗
PubMed2005

Ca2+-activated K+-current density is correlated with soma size in rat vestibular-afferent neurons in culture.

Vestibular-afferent neurons (VANs) transmit information about linear and angular accelerations during head movements from vestibular end organs to vestibular nuclei. In situ, these neurons show heterogeneous discharge patterns that may be produced by differences in their intrinsic properties. However, little is known about the ionic currents underlying their different firing patterns. Using the whole cell patch-clamp technique, we analyzed the expression of Ca(2+) and Ca(2+)-activated K(+) currents (I(KCa)) in primary cultured neurons isolated from young rats (p7-p10). We found two overlapping subpopulations of VANs classified according to low-threshold Ca(2+)-current [low-voltage-activated (LVA)] expression; LVA (-) neurons, formed by small cells, and LVA (+) neurons composed of medium to large cells. The I(KCa) in both cell-groups was carried through channels of high (BK), intermediate (IK), and low conductance (SK), besides a resistant channel to classical blockers (IR). BK was expressed preferentially in LVA (+) cells, whereas IR expression was preferentially in LVA (-) cells. No correlation between SK and IK expression with the soma size was found. Current-clamp experiments showed that BK participates in the adaptation of discharge and in the duration of the action potential, whereas SK and IK did not show a significant contribution to electrical discharge of cultured VANs. However, because of the low number of VANs in culture with repetitive firing it is difficult to interpret our results in terms of discharge patterns. Our results demonstrate that vestibular-afferent neurons possess different Ca(2+)-activated K(+) (K(Ca)) channels and that their expression, heterogeneous among the cells, would contribute to explain some of the differences in the electrical-firing properties of these neurons.

4-Aminopyridine↗
PubMed1996

Distribution of calcitonin gene-related peptide immunoreactivity in vestibular efferent neurons of the chinchilla.

The distribution of calcitonin gene-related peptide immunoreactivity (CGRPi) within efferent vestibular neurons in the chinchilla was investigated using fluorescent retrograde labeling combined with immunohistochemistry. Efferent vestibular neurons were found bilaterally in clusters: dorsolateral (group E1) and medial (group E2) to the genu of CN VII, as well as ventromedial to the descending CN VII fibers in the parvicellular reticular formation (PCR). The percentage of retrogradely labeled cells containing CGRPi was 77.1 +/- 5.7 for group E1 neurons, 90.3 +/- 3.8 in the E2 region. Among the PCR efferents more then half of the neurons (61.4 +/- 19.9%) expressed CGRP peptide or message. The wide distribution of CGRP among vestibular efferent neurons suggests that CGRP plays an important role in vestibular efferent function. In addition, the differential distribution among the groups of vestibular efferent neurons suggests that efferent modulation of vestibular function is different between the E cell group efferent neurons and the PCR efferent neurons.

Animals↗
PubMed2002

Intrinsic firing dynamics of vestibular nucleus neurons.

Individual brainstem neurons involved in vestibular reflexes respond to identical head movements with a wide range of firing responses. This diversity of firing dynamics has been commonly assumed to arise from differences in the types of vestibular nerve inputs to vestibular nucleus neurons. In this study we show that, independent of the nature of inputs, the intrinsic membrane properties of neurons in the medial vestibular nucleus substantially influence firing response dynamics. Hyperpolarizing and depolarizing inputs evoked a markedly heterogenous range of firing responses. Strong postinhibitory rebound firing (PRF) was associated with strong firing rate adaptation (FRA) and occurred preferentially in large multipolar neurons. In response to sinusoidally modulated input current, these neurons showed a pronounced phase lead with respect to neurons lacking strong PRF and FRA. A combination of the hyperpolarization-activated H current and slow potassium currents contributed to PRF, whereas FRA was predominantly mediated by slow potassium currents. An integrate-and-fire-type model, which simulated FRA and PRF, reproduced the phase lead observed in large neurons and showed that adaptation currents were primarily responsible for variations in response phase. We conclude that the heterogeneity of firing dynamics observed in response to head movements in intact animals reflects intrinsic as well as circuit properties.

Adaptation, Physiological↗
PubMed1980

Locus coeruleus-induced inhibition of dorsal cochlear nucleus neurons in comparison with lateral vestibular nucleus neurons.

The effects of conditioning stimulation of the locus coeruleus (LC) on the neuron activity of dorsal cochlear nucleus (DCN), which is rich in noradrenergic nerve terminals, were compared with those on the lateral vestibular nucleus (LVN), devoid of such terminals, to determine whether or not noradrenaline is responsible for the LC-induced inhibition. The conditioning stimuli applied to the LC had no effect on either the field potential or the spike generation of mono- and polysynaptic neurons in the LVN elicited by VIIIth cranial nerve stimulation. In contrast, the spike firing of the DCN neurons with VIIIth cranial nerve stimulation was significantly inhibited by LC conditioning stimulation. The inhibition of spike generation was mainly observed in the DCN neurons which fired spikes with a longer latency. The inhibition of DCN neurons by LC conditioning stimulation did not occur in the cats pretreated with reserpine; however, a rapid recovery of the inhibition was produced by intraventricular application of noradrenaline. These results are in good agreement with the histochemical findings and support our previous conclusion that noradrenaline acts as an inhibitory transmitter or modulator on the nuclei where noradrenergic nerve terminals derived from the LC are located. In addition, the vestibular input in the primary relay nucleus is apparently not regulated by noradrenaline originating in the LC.

Animals↗
PubMed2003

Long-term plasticity of ipsilesional medial vestibular nucleus neurons after unilateral labyrinthectomy.

Unilateral labyrinthectomy results in oculomotor and postural disturbances that regress in a few days during vestibular compensation. The long-term (after 1 mo) consequences of unilateral labyrinthectomy were investigated by characterizing the static and dynamic membrane properties of the ipsilesional vestibular neurons recorded intracellularly in guinea pig brain stem slices. We compared the responses of type A and type B medial vestibular nucleus neurons identified in vitro to current steps and ramps and to sinusoidal currents of various frequencies. All ipsilesional vestibular neurons were depolarized by 6-10 mV at rest compared with the cells recorded from control slices. Both their average membrane potential and firing threshold were more depolarized, which suggests that changes in active conductances compensated for the loss of excitatory afferents. The afterhyperpolarization and discharge regularity of type B but not type A neurons were increased. All ipsilesional vestibular cells became more sensitive to current injections over a large range of frequencies (0.2-30 Hz), but this increase in sensitivity was greater for type B than for type A neurons. This was associated with an increase of the peak frequency of linear response restricted to type B neurons, from 4-6 to 12-14 Hz. Altogether, we show that long-term vestibular compensation involves major changes in the membrane properties of vestibular neurons on the deafferented side. Many of the static and dynamic membrane properties of type B neurons became more similar to those of type A neurons than in control slices, leading to an increase in the overall homogeneity of medial vestibular nucleus neurons.

Action Potentials↗
PubMed2005

Immunocytochemical and stereological study of glucocorticoid receptors in rat medial vestibular nucleus neurons and the effects of unilateral vestibular deafferentation.

CONCLUSION: The results of this study suggest that neither the number of medial vestibular nucleus (MVN) neurons expressing cytosolic glucocorticoid receptors nor blood corticosterone levels change significantly during the development of vestibular compensation. OBJECTIVE: Vestibular compensation is a process of partial behavioral recovery that occurs following damage to the vestibular labyrinth. It has been suggested that this compensation process might be dependent on the release of glucocorticoids such as corticosterone at the time of unilateral vestibular deafferentation (UVD) and that changes in glucocorticoid receptors in the MVN might contribute to the initiation of the compensation process. MATERIAL AND METHODS: We compared the number of MVN neurons expressing cytosolic glucocorticoid receptors in rats at 10 h and 2 weeks following UVD, and in sham and anesthetic control animals; we also measured blood corticosterone levels. RESULTS: Using immunocytochemistry and stereology, we found that the majority of MVN neurons expressed glucocorticoid receptors, but there were no significant differences in the number of glucocorticoid receptor-expressing neurons in the ipsilateral or contralateral MVNs at 10 h or 2 weeks post-UVD; furthermore, corticosterone levels did not vary significantly between the UVD and control groups.

Adaptation, Physiological↗