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At least 19 recordsLinked to original sources
PubMed2006

Changes in protein expression in the rat medial vestibular nuclei during vestibular compensation.

The molecular mechanisms of neural and synaptic plasticity in the vestibular nuclei during 'vestibular compensation', the behavioural recovery that follows deafferentation of one inner ear, are largely unknown. In this study we have used differential proteomics techniques to determine changes in protein expression in ipsi-lesional and contra-lesional medial vestibular nuclei (MVN) of rats, 1 week after either sham surgery or unilateral labyrinthectomy (UL). A systematic comparison of 634 protein spots in two-dimensional electrophoresis gels across five experimental conditions revealed 54 spots, containing 26 proteins whose level was significantly altered 1 week post-UL. The axon-guidance-associated proteins neuropilin-2 and dehydropyriminidase-related protein-2 were upregulated in the MVN after UL. Changes in levels of further specific proteins indicate a coordinated upregulation of mitochondrial function, ATP biosynthesis and phosphate metabolism in the vestibular nuclei 1 week post-UL. These may reflect the metabolic energy demands of processes such as gliosis, neuronal outgrowth and synaptic remodelling that occur after UL. Our findings suggest novel roles for axon elaboration and guidance molecules, as well as mitochondrial and metabolic regulatory proteins, in the post-lesional physiology of the MVN during vestibular system plasticity.

Adaptation, Physiological↗
PubMed1999

Changes in protein expression in the vestibular nuclei during vestibular compensation.

In the guinea pig, labyrinthectomy induces an immediate depression of the resting discharges in the neurons of the ipsilateral vestibular nuclei. Later on, in spite of the persistent deprivation of their ipsilateral labyrinthine input, a spontaneous restoration of activity, which is complete within 1 week, occurs in these neurons. Here, by using computer-assisted quantitative two-dimensional gel analysis, we have detected three proteins whose expressions were increased in the ipsilateral vestibular nuclei 1 week after unilateral labyrinthectomy. The spatio-temporal pattern of this phenomenon was compatible with a role for it in the restoration of activity in the vestibular neurons deprived of their ipsilateral labyrinthine input. Furthermore, the N-terminal amino acid sequences of two of these expressed proteins were obtained.

Animals↗
PubMed1979

Visual modulation of otolith-dependent units in cat vestibular nuclei.

Vestibular nucleus units responding to translational self-motion are shown to respond also to translational movement of a large visual field. These visual-vestibular interactions in otolith-dependent units are similar to those found in canal-related units and could provide the basis for linearvection.

Animals↗
PubMed1989

Ipsilateral and contralateral projections to the trochlear nucleus arise from different subdivisions in the vestibular nuclei.

Vestibular neurons that project to the trochlear nucleus were studied following unilateral injections of horseradish peroxidase. After 48 h, the animals were perfused, transverse sections were cut, and reacted with diaminobenzidine. After injections centered on the trochlear nucleus, one-third of the labeled neurons were located in the ipsilateral superior (S) vestibular nucleus and almost half were in the contralateral medial (M) vestibular nucleus. Labeled fibers were restricted to the medial longitudinal fasciculus ipsilateral to the injection. This study supports hypotheses, based on physiological data of two vertical vestibulo-ocular pathways; one originating in the ipsilateral S that may be inhibitory and the second originating predominantly from the contralateral M that may be excitatory.

Afferent Pathways↗
PubMed2003

Organization of projections from the raphe nuclei to the vestibular nuclei in rats.

Previous anatomic and electrophysiological evidence suggests that serotonin modulates processing in the vestibular nuclei. This study examined the organization of projections from serotonergic raphe nuclei to the vestibular nuclei in rats. The distribution of serotonergic axons in the vestibular nuclei was visualized immunohistochemically in rat brain slices using antisera directed against the serotonin transporter. The density of serotonin transporter-immunopositive fibers is greatest in the superior vestibular nucleus and the medial vestibular nucleus, especially along the border of the fourth ventricle; it declines in more lateral and caudal regions of the vestibular nuclear complex. After unilateral iontophoretic injections of Fluoro-Gold into the vestibular nuclei, retrogradely labeled neurons were found in the dorsal raphe nucleus (including the dorsomedial, ventromedial and lateral subdivisions) and nucleus raphe obscurus, and to a minor extent in nucleus raphe pallidus and nucleus raphe magnus. The combination of retrograde tracing with serotonin immunohistofluorescence in additional experiments revealed that the vestibular nuclei receive both serotonergic and non-serotonergic projections from raphe nuclei. Tracer injections in densely innervated regions (especially the medial and superior vestibular nuclei) were associated with the largest numbers of Fluoro-Gold-labeled cells. Differences were observed in the termination patterns of projections from the individual raphe nuclei. Thus, the dorsal raphe nucleus sends projections that terminate predominantly in the rostral and medial aspects of the vestibular nuclear complex, while nucleus raphe obscurus projects relatively uniformly throughout the vestibular nuclei. Based on the topographical organization of raphe input to the vestibular nuclei, it appears that dense projections from raphe nuclei are colocalized with terminal fields of flocculo-nodular lobe and uvula Purkinje cells. It is hypothesized that raphe-vestibular connections are organized to selectively modulate processing in regions of the vestibular nuclear complex that receive input from specific cerebellar zones. This represents a potential mechanism whereby motor activity and behavioral arousal could influence the activity of cerebellovestibular circuits.

Animals↗
PubMed2002

Calcium-binding proteins map the postnatal development of rat vestibular nuclei and their vestibular and cerebellar projections.

We investigated whether three calcium-binding proteins, calretinin, parvalbumin, and calbindin, could identify specific aspects of the postnatal development of the rat lateral (LVN) and medial (MVN) vestibular nuclei and their vestibular and cerebellar connections. Calretinin levels in the vestibular nuclei, increased significantly between birth and postnatal day (P) 45. In situ hybridization and immunocytochemical staining showed that calretinin-immunoreactive neurons were mostly located in the parvocellular MVN at birth and that somatic and dendritic growth occurred between birth and P14. During the first week, parvalbumin-immunoreactive fibers and endings were confined to specific areas, i.e., the ventral LVN and magnocellular MVN, and identified exclusively the maturation of the vestibular afferents. Calbindin was located within the dorsal LVN and the parvocellular MVN and identified the first arrival of the corticocerebellar afferents. From the second week, in addition to labeling vestibular afferents in their specific target areas, parvalbumin was also found colocalized with calbindin in mature Purkinje cell afferents. Thus, the specific spatiotemporal distribution of parvalbumin and calbindin could correspond to two successive phases of synaptic remodeling involving integration of the vestibular sensory messages and their cerebellar control. On the basis of the sequence of distribution patterns of these proteins during the development of the vestibular nuclei, calretinin is an effective marker for neuronal development of the parvocellular MVN, parvalbumin is a specific marker identifying maturation of the vestibular afferents and endings, and calbindin is a marker of the first appearance and development of Purkinje cell afferents.

Animals↗
PubMed1989

Oculomotor functions of the flocculus and the vestibular nuclei after bilateral vestibular neurectomy.

Ito's hypothesis of an important role of the flocculus of the vestibulocerebellum in the immediate visual control of the VOR during visual-vestibular interaction has received substantial support. Nevertheless, several parts in this hypothesis are unclear, at least in primates. In normal monkey, vestibularly driven neurones in the vestibular nuclei do not carry signals which are adequate to account for the full range of eye movement responses during optokinetic tracking (OKN) and different situations of visual-vestibular interaction (especially VOR-suppression). Thus these neurones seem not to be located at the final stage where floccular "gaze-velocity" Purkinje cells (PCs) exert their control function on the three-neurone-reflex arc. The signals of these "central" vestibular neurones (if relevant for the oculomotor output) must further be processed. After bilateral vestibular neurectomy (BVN) only a small number of vestibular nuclei neurones were found with eye velocity sensitivities during smooth pursuit tracking (SP) and OKN in the range of those of floccular PCs (also after BVN), and with the appropriate polarity of modulation. Our difficulties in finding neurones in the vestibular nuclei which, according to their neurophysiological behaviour, could be main target cells of floccular PCs, either in normal or in BVN monkeys, are discussed.

Action Potentials↗
PubMed2006

The anatomy of the vestibular nuclei.

The vestibular portion of the eighth cranial nerve informs the brain about the linear and angular movements of the head in space and the position of the head with respect to gravity. The termination sites of these eighth nerve afferents define the territory of the vestibular nuclei in the brainstem. (There is also a subset of afferents that project directly to the cerebellum.) This chapter reviews the anatomical organization of the vestibular nuclei, and the anatomy of the pathways from the nuclei to various target areas in the brain. The cytoarchitectonics of the vestibular brainstem are discussed, since these features have been used to distinguish the individual nuclei. The neurochemical phenotype of vestibular neurons and pathways are also summarized because the chemical anatomy of the system contributes to its signal-processing capabilities. Similarly, the morphologic features of short-axon local circuit neurons and long-axon cells with extrinsic projections are described in detail, since these structural attributes of the neurons are critical to their functional potential. Finally, the composition and hodology of the afferent and efferent pathways of the vestibular nuclei are discussed. In sum, this chapter reviews the morphology, chemoanatomy, connectivity, and synaptology of the vestibular nuclei.

Animals↗
PubMed1983

Flocculectomy and unit activity in the vestibular nuclei during visual-vestibular interactions.

Activity of neurons in the vestibular nuclei of alert monkeys was recorded extracellularly after total unilateral and bilateral flocculectomy and partial paraflocculectomy. Type 1 horizontal cells that were encountered after flocculectomy responded to visual and vestibular stimuli and to conflict stimulation, i.e., to rotation in a subject-stationary visual surround, as do vestibular neurons in the normal animal. The major difference between neurons in the normal and lesioned animals was that more time was needed to reach steady state firing levels during optokinetic stimulation at a constant velocity after operation. As shown previously (Waespe et al. 1983) the longer time course is related to increased initial retinal slip velocities that occur after flocculectomy as a result of an inability to change eye velocity rapidly in response to visual stimulation. It does not signify a change in the dynamics of neurons in the vestibular nuclei that mediate the vestibulo-ocular reflex (VOR). The similarity in modulation of horizontal Type 1 vestibular neurons in normal and flocculectomized monkeys makes it unlikely that floccular Purkinje cells suppress the horizontal VOR in the monkey during conflicting visual and vestibular stimuli by inhibiting or disfacilitating secondary or tertiary vestibular neurons. This is consistent with earlier findings that indicate that visual-oculomotor pathways responsible for ocular pursuit or for rapid changes in OKN do not go through the vestibular nuclei. Rather the point of interaction of the flocculus output with the VOR appears to be external to the vestibular nuclei. There was a close correspondence between the slow phase velocity of nystagmus and unit activity in the vestibular nuclei under a wide variety of test conditions after flocculectomy. This is consistent with the postulate that frequencies of vestibular nuclei neurons represent a summation of activity in direct vestibulo-oculomotor pathways and indirect pathways that include the velocity storage mechanism. These are the major remaining sources of activity that generate slow phases of nystagmus after the direct visual-oculomotor pathways have been partially interrupted by flocculectomy (Waespe et al. 1983). Horizontal Type 1 neurons which responded to vestibular and optokinetic stimulation with increases in frequency above 1 spike/s/degree/s were rarely encountered after flocculectomy. These cells were present on the normal side in a monkey after unilateral flocculectomy. We infer that vestibular nuclei neurons that project mossy fibers to the flocculus are inactivated or disappear as a result of surgical ablation of their axons. This could also contribute to the reduced gain of vestibular nystagmus, OKAN and off-vertical nystagmus that was observed in some of the animals after lesion.

Animals↗
PubMed1984

Neuron activity in monkey vestibular nuclei during vertical vestibular stimulation and eye movements.

To elucidate how information is processed in the vestibuloocular reflex (VOR) pathways subserving vertical eye movements, extracellular single-unit recordings were obtained from the vestibular nuclei of alert monkeys trained to track a visual target with their eyes while undergoing sinusoidal pitch oscillations (0.2-1.0 Hz). Units with activity related to vertical vestibular stimulation and/or eye movements were classified as either vestibular units (n = 53), vestibular plus eye-position units (n = 30), pursuit units (n = 10), or miscellaneous units (n = 5), which had various combinations of head- and eye-movement sensitivities. Vestibular units discharged in relation to head rotation, but not to smooth eye movements. On average, these units fired approximately in phase with head velocity; however, a broad range of phase shifts was observed. The activities of 8% of the vestibular units were related to saccades. Vestibular plus eye-position units fired in relation to head velocity and eye position and, in addition, usually to eye velocity. Their discharge rates increased for eye and head movements in opposite directions. During combined head and eye movements, the modulation in unit activity was not significantly different from the sum of the modulations during each alone. For saccades, the unit firing rate either decreased to zero or was unaffected. Pursuit units discharged in relation to eye position, eye velocity, or both, but not to head movements alone. For saccades, unit activity usually either paused or was unaffected. The eye-movement-related activities of the vestibular plus eye-position and pursuit units were not significantly different. A quantitative comparison of their firing patterns suggests that vestibular, vestibular plus eye-position, and pursuit neurons in the vestibular nucleus could provide mossy fiber inputs to the flocculus. In addition, the vertical vestibular plus eye-position neurons have discharge patterns similar to those of fibers recorded rostrally in the medial longitudinal fasciculus. Therefore, our data support the view that vertical vestibular plus eye-position neurons are interneurons of the VOR.

Animals↗
PubMed2001

Current concepts of vestibular nucleus function: transformation of vestibular signals in the vestibular nuclei.

The vestibular nerve sends signals to the brain that code the movement and position of the head in space. These signals are used for a variety of functions, including the control of reflex and voluntary movements and the construction of a sense of self-motion. In order to carry out these functions, sensory vestibular signals need to be transformed in a variety of ways. Transformations are thought to occur at an early stage of sensory processing in the brain, and in many cases are apparent in the responses of neurons in the vestibular nuclei that receive direct inputs from the vestibular nerve. Several specific examples of sensory transformation in the vestibular nuclei are presented, and current hypotheses about the mechanisms that are used to produce the transformations are discussed.

Adaptation, Physiological↗
PubMed1977

Vestibular and somatosensory interaction in the cat vestibular nuclei.

The vestibular nuclei of cats were explored extracellulary with micropipettes to locate units with a resting discharge rate which responded to rotation in the horizontal plane. These units were examined for somatosensory input from neck and limbs. Fewer than half responded to somatosensory stimulation. The neck region was the body area most effective in influencing unitary activity. The response pattern most often noted was an increase and decrease in discharge frequency when the body was moved towards and away from the recording electrode respectively. Change in discharge rate was observed to be primarily dependant upon neck velocity and not upon absolute neck position. Half of the somatosensory units received input from either the forelimbs or the hindlimbs, while the remaining half responded to both.

Action Potentials↗
PubMed1996

Temporal relationship between the expression of fos, jun and krox-24 in the guinea pig vestibular nuclei during the development of vestibular compensation for unilateral vestibular deafferentation.

Immediately following unilateral vestibular deafferentation (UVD), expression of the c-fos protein increased in both vestibular nucleus complexes (VNCs). By 10 h post-UVD, c-fos proteins were more evident in the bilateral medial vestibular nuclei (MVN), but their expression had decreased in the bilateral superior vestibular nuclei (SVN) and lateral vestibular nuclei (LVN) compared to immediately post-UVD. At 50 h post-UVD, c-fos protein expression was still evident in the bilateral VNC, but had decreased relative to immediately post-UVD. Immediately post-UVD, c-jun protein expression increased in the bilateral VNC, but was more noticeable at 10 h post-UVD. By 50 h post-UVD, c-jun protein expression had decreased markedly throughout the bilateral VNC. The krox-24 protein could not be seen anywhere in the immediate post-UVD condition. However, it was expressed at a low level in the bilateral MVN at 10 h post-UVD; by 50 h post-UVD, this expression had decreased. No evidence of apoptosis was observed following UVD.

Adaptation, Physiological↗
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↗
PubMed2001

Gamma amino butyric acid (GABA) immunoreactivity in the vestibular nuclei of normal and unilateral vestibular neurectomized cats.

Recent neurochemical investigations of the central vestibular pathways have demonstrated that several neurotransmitters are involved in various operations required for stabilizing posture and gaze. Neurons of the vestibular nuclei (VN) receive GABAergic inhibitory afferents, and GABAergic neurons distributed throughout the vestibular complex are implicated in inhibitory vestibulo-ocular and vestibulo-spinal pathways. The aim of this study was to analyse the modifications of GABA immunoreactivity (GABA-ir) in the cat VN after unilateral vestibular neurectomy (UVN). Indeed, compensation of vestibular deficits is a good model for studying adult central nervous system (CNS) plasticity and the GABAergic system is involved in CNS plasticity. We studied GABA-ir by using a purified polyclonal antibody raised against GABA. Light microscopic preparations of thin (20 microm) sections of cat VN were used to quantify GABA-ir by an image analysing system measuring GABA-positive punctate structures and the number of GABA-positive neurons. Both the lesioned and intact sides were analysed in three populations of UVN cats killed at different times after injury (1 week, 3 weeks and 1 year). These data were compared to those collected in normal unlesioned and sham-operated cats. Results showed a spatial distribution of GABA-ir in the control cats that confirmed previous studies. GABA-ir neurons, fibres and nerve terminals were scattered in all parts of the VN. A higher concentration of GABA-positive neurons (small cells) was detected in the medial and inferior VN (MVN and IVN) and in the dorsal part of the lateral VN (LVNd). A higher level of GABA-positive punctate structures was observed in the MVN and in the prepositus hypoglossi (PH) nucleus. Lesion-induced changes were found at each survival time. One week after injury the number of GABA-positive neurons was significantly increased in the MVN, the IVN and the dorsal part of the LVN on the lesioned side and in the ventral part of the LVN on the intact side. One year later a bilateral increase in GABA-positive neurons was detected in the MVN whilst a bilateral decrease was observed in both the SVN and the ventral part of the LVN. Changes in the GABA-staining varicosities did not strictly coincide with the distribution of GABA-ir cells, suggesting that GABA-ir fibres and nerve terminals were also modified. One week and later after injury, higher GABA-staining varicosities were seen unilaterally in the ipsilateral MVN. In contrast, bilateral increases (in PH) and bilateral decreases (in SVN and the ventral part of the LVN) were recorded in the nearly (3 weeks) or fully (1 year) compensated cats. At this stage GABA-staining varicosities were significantly increased in the lesioned side of the MVN. These findings demonstrate the reorganization of the GABAergic system in the VN and its possible role in recovery process after UVN in the cat. The changes seen during the acute stage could be causally related to the VN neuron deafferentation, contributing to the static vestibular deficits. Those found in the compensated cats would be more functionally implicated in the dynamic aspects of vestibular compensation.

Adaptation, Physiological↗