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PubMedDate not supplied

Development of a biophysical model for vestibular prosthesis research.

Physiologic properties of primary vestibular neurons are compared and contrasted with properties of primary auditory neurons. The differences and similarities suggest possible coding strategies for a vestibular implant. The degree of spike rate variability, or coefficient of variation (CV), is a prominent physiological property of vestibular neurons with undetermined functional significance. At the very least, CV is highly correlated with threshold to electrical stimulation in the intact vestibular labyrinth. If CV is also important for vestibular coding, then electrical stimulation strategies should be designed to restore relatively physiologic patterns of CV. Simulations using a stochastic model of primary afferent vestibular neurons reveal that this should be possible using combinations of low and high-rate pulsatile stimulation. They also demonstrate that differences in the number and independence of synaptic inputs can significantly affect CV.

Action Potentials↗

PubMed2000

Sensory processing in the vestibular nuclei during active head movements.

Many secondary vestibular neurons are sensitive to head on trunk rotation during reflex-induced and voluntary head movements. During passive whole body rotation the interaction of head on trunk signals related to the vestibulo-collic reflex with vestibular signals increases the rotational gain of many secondary vestibular neurons, including many that project to the spinal cord. In some units, the sensitivity to head on trunk and vestibular input is matched and the resulting interaction produces an output that is related to the trunk velocity in space. In other units the head on trunk inputs are stronger and the resulting interaction produces an output that is larger during the reflex. During voluntary head movements, inputs related to head on trunk movement combine destructively with vestibular signals, and often cancel the sensory reafferent consequences of self-generated movements. Cancellation of sensory vestibular signals was observed in all of the antidromically identified secondary vestibulospinal units, even though many of these units were not significantly affected by reflexive head on trunk movements. The results imply that the inputs to vestibular neurons related to head on trunk rotation during reflexive and voluntary movements arise from different sources. We suggest that the relative strength of reflexive head on trunk input to different vestibular neurons might reflect the different functional roles they have in controlling the posture of the neck and body.

Animals↗

PubMed1996

Effects of substance P on medial vestibular nucleus neurons in guinea-pig brainstem slices.

The undecapeptide substance P (SP) has been recently implicated in the control of vestibular function. In particular, it seems to be co-localized with glutamate in approximately half of the primary vestibular afferents in mammals. Using intracellular recordings in guinea-pig brainstem slices, we have investigated the effects of SP and of several agonists of the three known tachykinin receptor subtypes (NK1, NK2 and NK3) on the three main types (A, B and B+LTS) of guinea-pig medial vestibular nucleus neurons (MVNn) that we had previously described. SP could induce two distinct kinds of effects on all types of MVNn. Whereas around half of them were depolarized and had their membrane resistance increased by SP, approximately 10% of all MVNn were in contrast hyperpolarized and inhibited while their membrane resistance was decreased. Both responses persisted under conditions of blockade of synaptic transmission, and were thus due to the activation of postsynaptic binding sites. The SP-induced membrane depolarization could not be reproduced with any one of the specific agonists of the three tachykinin receptor subtypes, nor was it blocked by the specific NK1 receptor antagonists GR 82664 and CP 99994. This effect might therefore be due to the activation of a new, pharmacologically distinct, 'NK1-like' receptor. Only the hyperpolarizing effects, which were in contrast mimicked by the specific NK1 receptor agonists GR 73632 and [Sar9, Met (O2)11]-SP, would be mediated by the few typical NK1 receptors which have been demonstrated in the medial vestibular nucleus.

Animals↗

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↗

PubMed1995

Role of glucocorticoid in vestibular compensation in relation to activation of vestibular nucleus neurons.

It is still not established whether or not glucocorticoids are effective in the treatment of vestibular disorders such as dizziness and imbalance, although these drugs in combination with several others are used to treat dizziness and imbalance in some diseases. This study was undertaken to investigate the effects of a glucocorticoid, dexamethasone, on vestibular disorder following unilateral labyrinthectomy in pigmented rabbits. Neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats were also investigated. Systemic injection of dexamethasone decreased the frequency of nystagmus and head deviation dose-dependently following hemilabyrinthectomy, and the rate of decrease was faster than that obtained by saline. In contrast, RU38486 (a glucocorticoid receptor antagonist) delayed the reduction of nystagmus and head deviation. Micro-iontophoretic application of dexamethasone rapidly enhanced the spontaneous firing of MVN neurons in a dose-dependent manner. These increases were blocked by RU38486, but not by GDEE (a glutamate receptor antagonist) or Co2+ (a Ca2+ channel blocker). These results suggest that dexamethasone directly activates the MVN neurons, thereby accelerating vestibular compensation.

Adaptation, Physiological↗

PubMed1992

Responses of vestibular and prepositus neurons to head movements during voluntary suppression of the vestibuloocular reflex.

Neurons in the vestibular nuclei and the prepositus nucleus exhibited several different types of changes in their firing behavior during voluntary cancellation of the horizontal VOR. The head velocity sensitivity of type I position-vestibular-pause neurons was reduced during cancellation, while type II vestibular neurons exhibit an increase in their sensitivity. The firing behavior of burst tonic neurons in the medial vestibular nucleus, the prepositus nucleus, like the cells in the abducens nucleus, was closely related to the eye movements generated when the VOR is cancelled. Other cells in the PH and MVN respond primarily to smooth pursuit eye movements. We suggest that the behavior of abducens neurons during the VOR and during VOR cancellation can be explained if they receive inputs from PVP neurons, burst tonic neurons, and smooth pursuit neurons.

Animals↗

PubMed1995

Glycinergic inhibition of spontaneously active guinea-pig medial vestibular nucleus neurons in vitro.

Effects of glycine on the spontaneous activity of medial vestibular nucleus (MVN) neurons recorded extracellularly from guinea-pig brainstem slices were investigated. Glycine produced a dose-dependent decrease in the resting discharge rate of all MVN neurons tested, with a mean EC50 of 3.9 x 10(-4) M. The inhibitory effect of glycine was reversibly blocked by strychnine and persisted in a low calcium/high magnesium-containing saline solution. These findings suggest the existence of a direct strychnine-sensitive inhibitory effect of glycine on guinea-pig MVN neurons.

Animals↗

PubMed1995

Neurotrophin-4/5, brain-derived neurotrophic factor, and neurotrophin-3 promote survival of cultured vestibular ganglion neurons and protect them against neurotoxicity of ototoxins.

The ability of neurotrophin-4/5 (NT-4/5), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and nerve growth factor (NGF) to promote survival of postnatal rat vestibular ganglion neurons (VGNs) was examined in dissociated cell cultures. Of the four neurotrophins, NT-4/5 and BDNF were equally effective but more potent than NT-3 in promoting the survival of VGNs. In contrast, NGF showed no detectable effects. As expected, TrkB-IgG (a fusion protein of extracellular domain of TrkB and Fc domain of human immunoglobulin G) specifically inhibited the survival-promoting, effects by NT-4/5 or BDNF and TrkC-IgG fusion protein completely blocked that of NT-3. Immunohistochemistry with TrkB, TrkA, and p75 antisera revealed that VGNs made TrkB and p75 proteins, but not TrkA protein. Ototoxic therapeutic drugs such as cisplatin and gentamicin often induce degeneration of hair cells and ganglion neurons in both auditory and vestibular systems that leads to impairment of hearing and balance. When cisplatin and gentamicin were added to the dissociated VGN culture in which the hair cells were absent, additional cell death of VGNs was induced, suggesting that the two ototoxins may have a direct neurotoxic effect on ganglion neurons in addition to their known toxicity on hair cells. However, if the cultures were co-treated with neurotrophins, NT-4/5, BDNF, and NT-3, but not NGF, prevented or reduced the neurotoxicity of the two ototoxins. Thus, the three neurotrophins are survival factors for VGNs and are implicated in the therapeutic prevention of VGN loss caused by injury and ototoxins.

Animals↗

PubMed1990

Inhibition by enkephalin of medial vestibular nucleus neurons responding to horizontal pendular rotation.

Electrophysiological studies were performed to determine whether or not enkephalin modulates the activities of medial vestibular nucleus (MVN) neurons responding to horizontal pendular rotation using alpha-chloralose anesthetized cats. The effects of microiontophoretically applied drugs were examined in type I and type II neurons identified according to responses to horizontal, sinusoidal rotation; type I and type II neurons showed an increase and decrease in firing with rotation ipsilateral to the recording site and vice versa with contralateral rotation, respectively. Iontophoretic application of enkephalin suppressed spike firing induced by rotation of the animals in type I neuron, but not in type II neuron. The spike firing induced by iontophoretically applied glutamate was also inhibited during the application of enkephalin. The inhibition by enkephalin of both rotation- and glutamate-induced firing was antagonized by naloxone which was given simultaneously. These results suggest that enkephalin acts on MVN type I neuron to inhibit transmission from the vestibule, thereby controlling vestibulo-ocular reflex.

Animals↗

PubMed1994

Ionic conductances contributing to spike repolarization and after-potentials in rat medial vestibular nucleus neurones.

1. Intracellular recordings were made from 123 tonically active medial vestibular nucleus (MVN) neurones in a horizontal slice preparation of the dorsal brainstem of the rat. On the basis of their averaged action potential shapes, the cells were classified as either type A, having a single deep after-hyperpolarization (AHP; 40/123 cells, 33%), or type B, having an early fast AHP and a delayed slow AHP (83/123 cells, 67%). The two cell types were distributed throughout the rostrocaudal extent of the MVN. 2. In type A cells TEA reduced the single deep AHP and decreased the rate of spike repolarization. Depolarizing current pulses from a hyperpolarized membrane potential elicited spikes with short plateau potentials in TEA. These persisted in Ca(2+)-free medium but were abolished along with the spontaneous activity in TTX. Ca(2+)-free medium did not affect the initial rate of repolarization but reduced the deep AHP. Apamin and carbachol had little effect. 4-Aminopyridine (4-AP) slowed spike repolarization and the AHP amplitude by a small amount. Thus, in type A cells spike repolarization and AHP appear to be mediated largely by a TEA-sensitive potassium current (presumably IK) and an apamin-insensitive Ca(2+)-activated potassium current (presumably IC). 3. The early fast AHP in type B cells was readily abolished in TEA. In seven of ten type B cells tested, the spontaneous spikes developed plateau potentials of 100-120 ms duration in 10 mM TEA, which then became 7-9 s long in Ca(2+)-free medium. In the remaining three cells, the spontaneous plateaux were 1.75-2 s long in TEA, and were reduced to 30-100 ms in Ca(2+)-free medium. TTX abolished the spontaneous spikes and plateaux. The delayed AHP was abolished by apamin, which induced irregular firing. 4-AP slowed spike repolarization and abolished the fast AHP, but did not induce plateaux. Thus, in type B cells spike repolarization involves a TEA-sensitive current (presumably IK) as well as IC and the 4-AP-sensitive potassium current IA, while the apamin-sensitive potassium current IAHP is responsible for the delayed AHP. 4. The tonic activity in type B cells appears to be regulated mainly by interactions between a persistent Na+ current, which in most cells is large enough to generate plateaux when repolarization is impeded in TEA, and the hyperpolarization mediated by IAHP. About 30% of type B cells have an additional inward Ca2+ current.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1993

Properties of superior vestibular nucleus neurons projecting to the cerebellar flocculus in the squirrel monkey.

1. Properties of superior vestibular nucleus (SVN) neurons and their projection to the cerebellar flocculus were studied in alert squirrel monkeys by using chronic unit and eye movement recording and microstimulation techniques. Twenty-three cells were antidromically activated from the ipsilateral flocculus, and seventeen of these were also orthodromically activated from the ipsilateral VIIth nerve at monosynaptic latencies. Only 1 of these 23 units was also inhibited by flocculus stimulation. According to their response properties, 9 of the cells were pure vestibular, 2 were vestibular-pause, and 12 were position-vestibular cells. The mean eye position sensitivity of these position-vestibular cells was significantly lower than that of cells projecting to the oculomotor nucleus (OMN). No eye movement-only neurons were antidromically activated from the flocculus. No cells could be antidromically activated from both the oculomotor nucleus and the flocculus.

Animals↗

PubMed2001

Inhibitory effects of tandospirone, a 5-HT1A agonist, on medial vestibular nucleus neurons responding to lateral roll tilt stimulation in rats.

An electrophysiological study was performed using chloral hydrate-anesthetized rats to determine whether tandospirone, a 5-HT1A agonist, affects neuronal activities of the medial vestibular nucleus (MVN), since serotonergic innervation and 5-HT1A receptors are present in this nucleus. Tandospirone applied microiontophoretically at a current of 20-60 nA caused an inhibition of tilt-induced firing of alpha-type neurons, which showed increased and decreased firing with lateral tilt ipsilateral and contralateral to the recording site, respectively, along with that of beta-type neurons which exhibited the reverse responses to ipsilateral and contralateral tilt stimulation. The inhibition was antagonized during simultaneous, iontophoretic application of WAY-100635 (20-60 nA), a 5-HT1A receptor antagonist, although WAY-100635 alone rarely affected spontaneous or tilt-induced firing in either type of neurons. These results suggest that tandospirone acts on a 5-HT1A receptor to inhibit transmission of otolith information to alpha- and beta-type MVN neurons.

Action Potentials↗

PubMed1999

Cholinergic and glutamatergic transmission in medial vestibular nucleus neurons responding to lateral roll tilt in rats.

The responses of the medial vestibular nucleus (MVN) neurons to lateral tilt and the neurotransmitters mediating otolith information to MVN neurons were investigated using rats. A computer-operated goniometer was tilted 20 degrees clockwise and counterclockwise at an angular speed of 5 degrees /s and paused in the inclined positions for 10 s to record neuronal responses in the static phase. The 185 MVN neurons recorded were classified into eight types according to their responses to tilt (alpha, beta, gamma, delta, epsilon, zeta, eta and theta). A majority showed increased firing in response to ipsilateral tilting and decreased firing in response to contralateral tilting (alpha type: 31.4%) or exhibited the reverse pattern (beta type: 36.8%). Further, other groups of neurons increased (gamma type) or decreased (delta type) firing rates to either side tilting and increased (epsilon and zeta type) or decreased (eta and theta type) firing only on one side. Atropine or L-glutamic acid diethyl ester hydrochloride (GDEE) applied microiontophoretically antagonized tilt-induced firing of alpha type neurons in 58.8% or 60.0%, respectively, and of beta type neurons in 66.7% or 58.3%, respectively. When the effects of atropine and GDEE were examined in the same neurons, antagonizing effects of both drugs on tilt-induced firing were obtained in 28.6% and 40.0% of alpha and beta type neurons, respectively. These results suggest that both acetylcholine and glutamate act as neurotransmitters in the transmission of otolith information to most MVN neurons.

Animals↗

PubMed2000

The normal distribution and projections of constitutive NADPH-d/NOS neurons in the brainstem vestibular complex of the rat.

The vestibular system is a highly conserved sensory system in vertebrates that is largely responsible for maintenance of one's orientation in space, posture, and balance and for visual fixation of objects during motion. In light of the considerable literature indicating an involvement of nitric oxide (NO) in sensory systems, it is important to determine whether NO is associated with vestibular pathways. To study the relationship of NO to vestibular pathways, we first examined the normal distribution of constitutive NADPH-diaphorase (NADPH-d), a marker for nitric oxide synthase (NOS), in the vestibular complex (VC) and then examined its association with selected vestibular projection neurons. Survey of the four major vestibular nuclei revealed that only the medial vestibular nucleus contained significant numbers of perikarya stained for NADPH-d/NOS. By contrast, all the vestibular nuclei contained a network of fine processes that stained positive for NADPH-d, although the density of this network varied among the individual nuclei. To determine whether NADPH-d/NOS neurons project to vestibular efferent targets, injections of the retrograde tracer Fluoro-Gold were made into known targets of second-order vestibular neurons. Vestibular neurons containing constitutive NADPH-d/NOS were found to project predominantly to the oculomotor nucleus. A small number of neurons also participate in vestibulothalamic and intrinsic vestibular connections. These results indicate that NADPH-d/NOS neurons are prevalent in the MVN and that a subpopulation of these neurons project to the oculomotor complex. Nitric oxide is probably released locally from axons located throughout the vestibular complex but may play a particularly important role in vestibulo-ocular pathways.

Animals↗

PubMed1991

Effects of anti-vertigo drugs on medial vestibular nucleus neurons activated by horizontal rotation.

The effects of anti-vertigo drugs on medial vestibular nucleus (MVN) neurons were examined to assess the site and mode of action using cats anesthetized with alpha-chloralose. Single neuron activity in the MVN was extracellularly recorded using a silver wire microelectrode attached along a seven-barreled micropipette, each of which was filled with diphenhydramine, diphenidol, betahistine, glutamate or NaCl. Type I of the MVN neurons were identified according to the responses obtained when the animal placed on a turn-table was rotated sinusoidally. The effects of the drugs were examined on type I neurons which received impulses primarily from the labyrinth and sent them to the oculomotor nuclei. The microiontophoretic application of diphenhydramine, diphenidol and betahistine inhibited rotation-induced firing of type I MVN neurons. Diphenhydramine and diphenidol were more potent than betahistine. These results suggest that these drugs directly act on MVN neurons to reduce the responsiveness to rotatory stimulation.

Animals↗

PubMedDate not supplied

Quantification of tracking eye movements in patients with neurological disorders.

Tracking eye movements were studied in 20 healthy subjects and in 24 patients with vestibular neuronitis, disorders within the frontal cortex, the cerebellum or the brain stem. The tracking tests were performed at six different target velocities between 10-60 degrees s-1 and different parameters were evaluated. The maximum velocity gain of smooth pursuit as normal in the group with vestibular neuronitis but reduced in the groups with disorders within the frontal cortex, cerebellum and the brain stem. The total amplitude of tracking and amplitude of smooth pursuit were normal in the groups with vestibular neuronitis and frontal cortical disorders, while in the groups with cerebellar and brain stem disorders it was reduced. The frequency of superimposed saccades with amplitude range of 3-10 degrees was significantly increased in all groups; however, in the group with vestibular neuronitis the increase was significant only during tracking in the direction of spontaneous nystagmus. The number of superimposed saccades with amplitude range of 11-20 degrees was significantly increased only in the group with cerebellar disorders. The frequency of square waves was not significantly increased in any group. Quantitative analysis of tracking eye movements seems to be a valuable aid for evaluation of site of lesions in the central nervus system.

Adolescent↗

PubMed2003

Central vestibular system: vestibular nuclei and posterior cerebellum.

The vestibular nuclei and posterior cerebellum are the destination of vestibular primary afferents and the subject of this review. The vestibular nuclei include four major nuclei (medial, descending, superior and lateral). In addition, smaller vestibular nuclei include: Y-group, parasolitary nucleus, and nucleus intercalatus. Each of the major nuclei can be subdivided further based primarily on cytological and immunohistochemical histological criteria or differences in afferent and/or efferent projections. The primary afferent projections of vestibular end organs are distributed to several ipsilateral vestibular nuclei. Vestibular nuclei communicate bilaterally through a commissural system that is predominantly inhibitory. Secondary vestibular neurons also receive convergent sensory information from optokinetic circuitry, central visual system and neck proprioceptive systems. Secondary vestibular neurons cannot distinguish between sources of afferent activity. However, the discharge of secondary vestibular neurons can distinguish between "active" and "passive" movements. The posterior cerebellum has extensive afferent and efferent connections with vestibular nuclei. Vestibular primary afferents are distributed to the ipsilateral uvula-nodulus as mossy fibers. Vestibular secondary afferents are distributed bilaterally. Climbing fibers to the cerebellum originate from two subnuclei of the contralateral inferior olive; the dorsomedial cell column and beta-nucleus. Vestibular climbing fibers carry information only from the vertical semicircular canals and otoliths. They establish a coordinate map, arrayed in sagittal zones on the surface of the uvula-nodulus. Purkinje cells respond to vestibular stimulation with antiphasic modulation of climbing fiber responses (CFRs) and simple spikes (SSs). The modulation of SSs is out of phase with the modulation of vestibular primary afferents. Modulation of SSs persists, even after vestibular primary afferents are destroyed by a unilateral labyrinthectomy, suggesting that an interneuronal network, triggered by CFRs is responsible for SS modulation. The vestibulo-cerebellum, imposes a vestibular coordinate system on postural responses and permits adaptive guidance of movement.

Acoustic Stimulation↗

PubMed1989

Neurofilament immunoreactivity in vestibular ganglion neurons of the adult rat.

Immunocytochemical methods were used to study the distribution of neurofilament (NF) proteins in vestibular ganglion neurons of the adult rat. Monoclonal antibodies against the three triplet proteins were used. By indirect immunofluorescence and the peroxidase-antiperoxidase method, two populations of neurons were distinguished. One population with large perikarya showed strong NF immunoreactivity. A second population of neurons presented only slight or no immunoreactivity. The strong NF immunoreactivity in the perikarya of certain neurons seems to be a general feature of many sensory ganglia.

Animals↗