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PubMed1999

Ultrastructure of vestibular commissural neurons related to velocity storage in the monkey.

The angular vestibulo-ocular reflex maintains gaze during head movements. It is thought to be mediated by two components: direct and velocity storage pathways. The direct angular vestibulo-ocular reflex is conveyed by a three neuron chain from the labyrinth to the ocular motoneurons. The indirect pathway involves a more complex neural network that utilizes a portion of the vestibular commissure. The purpose of the present study was to identify the ultrastructural characteristics of commissural neurons in the medial vestibular nucleus that are related to the velocity storage component of the angular vestibulo-ocular reflex. Ultrastructural studies of degenerating medial vestibular nucleus neurons were conducted in monkeys following midline section of rostral medullary commissural fibers with subsequent behavioral testing. After this lesion, oculomotor and vestibular functions attributable to velocity storage were abolished, whereas the direct angular vestibulo-ocular reflex pathway remained intact. Since this damage was functionally discrete, degenerating neurons were interpreted as potential participants in the velocity storage network. Ultrastructural observations indicate that commissural neurons related to velocity storage are small and medium sized cells having large nuclei with deep indentations and relatively little cytoplasm, which are located in the lateral crescents of rostral medial vestibular nucleus. The morphology of degenerating dendritic profiles varied. Some contained numerous round or tubular mitochondria in a pale cytoplasmic matrix with few other organelles, while others had few mitochondria but many cisterns and vacuoles in dense granular cytoplasm. The commissural nature of these cells was further suggested by the presence of two different types of degenerating axon terminals in the rostral medial vestibular nucleus: those with a moderate density of large spherical synaptic vesicles, and those with pleomorphic, primarily ellipsoid synaptic vesicles. The recognition of two types of degenerating terminals further supports our interpretation that at least two morphological types of commissural neurons participate in the velocity storage network. The degenerating boutons formed contacts with a variety of postsynaptic partners. In particular, synapses were observed between degenerating boutons and non-degenerating dendrites, and between intact terminals and degenerating dendrites. However, degenerating pre- and postsynaptic elements were rarely observed in direct contact, suggesting that additional neurons are interposed in the indirect pathway commissural system. On the basis of these ultrastructural observations, it is concluded that vestibular commissural neurons involved in the mediation of velocity storage have distinguishing ultrastructural features and synaptology, that are different from those of direct pathway neurons.

Animals↗
PubMed1999

Post-lesional plasticity in the central nervous system of the guinea-pig: a "top-down" adaptation process?

Vestibular compensation for the postural and oculomotor deficits following unilateral labyrinthectomy is a model of functional plasticity in the brain of adult vertebrates. The mechanisms involved in this recovery are still controversial. The post-lesional lack of vestibular input might be compensated by changes in the efficacy of the remaining sensory inputs involved in gaze and posture stabilization. However, the compensation process could also rapidly become independent of these external cues, and thus be detectable in vitro in preparations obtained from lesioned animals. In agreement with this hypothesis, we have shown recently that prominent traces of the compensation process appeared three days after the lesion on in vitro isolated brains taken from labyrinthectomized guinea-pigs, where the connectivity of the central vestibular-related networks is preserved. We report here that, one week after the lesion, a slight increase in the intrinsic, spontaneous activity of the deafferented, central vestibular neurons was found in brainstem slices. This increase became stronger in slices taken after one month of compensation, and was associated at this stage with a significant decrease in the intrinsic activity of the vestibular neurons on the contralesional side. Vestibular compensation could thus follow a "top-down" strategy: it would first rely on the external cues given by the intact sensory systems, then on an internal reorganization of the vestibular-related networks, and finally on changes in the intrinsic properties of the vestibular neurons themselves. Similar strategies may be used by the mammalian brain to compensate for other types of deafferentations or environmental changes.

Adaptation, Physiological↗
PubMed1992

Tonic activity of rat medial vestibular nucleus neurones in vitro and its inhibition by GABA.

The spontaneous discharge of 48 medial vestibular nucleus (MVN) neurones was recorded extracellularly in horizontal slices of the rat brainstem in vitro. The mean tonic rate of discharge was 17.1 +/- 8.2 imp/s, similar to that observed by others in transverse (coronal) slices of the rat and guinea pig MVN. The tonic rate of discharge of individual MVN cells either increased or decreased after synaptic blockade in low Ca2+ media, suggesting that ongoing synaptic activity has an important influence on the spontaneous activity of MVN cells in vitro. However the persistence of tonic activity after synaptic blockade indicates that an intrinsic, pacemaker-like mechanism is involved in the generation of the tonic activity. GABA, muscimol, baclofen and 3-APA inhibited the tonic activity of all MVN cells tested. Bicuculline antagonised, and picrotoxin blocked, the inhibitory responses to muscimol, but the effects of GABA were only partially blocked in 50 microM picrotoxin. The effects of baclofen and 3-APA persisted in low Ca2+ media, and were antagonised by saclofen and phaclofen. Picrotoxin-resistant responses to GABA persisted in low Ca2+ media, and were also antagonised by saclofen. These results suggest that the inhibitory control of MVN neurones by GABA involves both the GABAA and GABAB subtypes of GABA receptor. GABAB receptors appear to be distributed both pre- and post-synaptically in the rat MVN. The possible significance of the intrinsic, tonic activity of MVN cells in normal vestibular function and in vestibular compensation, and the effects of GABA, are discussed.

Action Potentials↗
PubMed1990

Guinea pig medial vestibular nucleus neurons in vitro respond to ACTH4-10 at picomolar concentrations.

The responses of single guinea pig medial vestibular nucleus (MVN) neurons in vitro to adrenocorticotropic hormone, fragment 4-10 (ACTH4-10) were recorded extracellularly. In coronal slices and in the isolated MVN, neurons were found which responded to ACTH4-10 at picomolar concentrations (10(-12)M), indicating that ACTH4-10 acts directly on MVN neurons and suggesting the possibility that ACTH4-10 may act as a neurotransmitter in the MVN. In most cases where neurons responded to ACTH4-10 (37/74 neurons), the effect was a decrease in firing. Whether or not the depressive action of ACTH4-10 on the firing rate of MVN neurons in vitro is related to the acceleration of behavioral recovery from unilateral labyrinthectomy (vestibular compensation), which has been reported previously (Flohr and Luneburg 1982; Igarashi et al. 1985), is unclear.

Adrenocorticotropic Hormone↗
PubMed1994

Up-regulation of GAP-43 (B50/F1) gene expression in vestibular efferent neurons following labyrinthectomy in the rat: in situ hybridization using an alkaline phosphatase-labeled probe.

Growth-associated protein (GAP)-43 plays a significant role in nerve regeneration and synaptic remodeling. We examined the profiles of GAP-43 mRNA expression in vestibular efferent neurons after labyrinthectomy in adult rats, and clearly demonstrated that labyrinthectomy increased GAP-43 expression in these neurons. This finding suggests the ability of vestibular efferent nerves to regenerate after nerve injury.

Alkaline Phosphatase↗
PubMed1997

Diverse effects of Purkinje cell loss on deep cerebellar and vestibular nuclei neurons in Purkinje cell degeneration mutant mice: a possible compensatory mechanism.

The genetic defect in the Purkinje cell degeneration (PCD) mutant mouse completely disrupts the cerebellar corticonuclear connection through intrinsic action on the final integrating unit of the cerebellar cortex, the Purkinje cell (PC). The postsynaptic target neurons of the PC in the deep cerebellar nuclei (DCN) and the vestibular nuclei (VN) are denervated by this PC loss by more than two-thirds of their total y-aminobutyric acid (GABA)-ergic innervation. This massive disinhibition should be reflected in an increased and thus electrophysiologically detectable activity of the respective neurons. To address this question, we performed extracellular recordings of PCD mutant and corresponding wild-type VN neurons under sinusoidal vestibular stimulation. The response amplitudes (neuronal response to sinusoidal rotation) of VN neurons in PCD mutant mice showed a decrease rather than the expected increase. The same was true for the mean resting rate, whereas the phase relationships were unaffected for the most part. This finding is a clear indication of compensatory reactions in the VN that substitute quantitatively for the lost PC inhibition. The expression of the calcium-binding protein parvalbumin (Parv) is assumed to correlate with the physiological activity of neurons, and Parv is localized predominantly in inhibitory neurons. Because inhibitory inter- or projecting neurons are also largely denervated by the PC loss, Parv immunocytochemistry also was performed. In wild-type mice, only very few Parv-immunopositive (Parv+) somata were present in the VN, and none were present in the DCN. In PCD mutant mice, a substantial number of Parv+ neuronal somata were visible in the VN, and even more were visible in the DCN. This increase in Parv+ somata in PCD mutant mice is closely related temporally and spatially to the extent of denervation caused by the PCD. Parv+ neuronal somata are first visible in the dentate nucleus at postnatal day (P) 24 and appear in the other cerebellar and VN up to P29. Direct double labeling of Parv and GABA and of Parv and glycine reveals that the large majority of Parv + neurons colocalize GABA, glycine, or both inhibitory transmitters. These results show that neurons that are postsynaptic to cerebellar PC develop diverse physiological and biochemical reactions in the course of genetically determined PCD. These mechanisms are likely to contribute to the phenotypically mild motor disturbances observed in PCD mutant mice.

Animals↗
PubMed2004

Nitric oxide increases the spontaneous firing rate of rat medial vestibular nucleus neurons in vitro via a cyclic GMP-mediated PKG-independent mechanism.

The effects of nitric oxide (NO) on the discharge rate of medial vestibular nucleus neurons (MVNn) were investigated in rat brainstem slices. The NO-donor sodium nitroprusside (SNP, 200 microM) caused a marked enhancement (+36.7%) of MVNn spontaneous firing rate, which was prevented by the NO-scavenger, carboxy-PTIO (300 microM). The SNP effects were not modified (+37.4%) by synaptic uncoupling, suggesting that NO influences intrinsic membrane properties of MVNn rather than the synaptic input they receive. The excitatory action of SNP was virtually abolished by slice pretreatment with the soluble guanylyl cyclase inhibitor, ODQ (10 microM), and it was mimicked (+33.1%) by the cGMP analogue 8-Br-cGMP (400 microM). Protein kinase G (PKG) and cAMP/protein kinase A (PKA) were both excluded as downstream effectors of the NO/cGMP-induced excitation. However, the cyclic nucleotide-gated (CNG) channel blockers, L-cis-diltiazem (LCD, 100 microM) and Sp-8-Br-PET-cGMPS (100 microM), significantly reduced the firing rate increase produced by 8-Br-cGMP. Moreover, LCD alone decreased spontaneous MVNn firing (-19.7%), suggesting that putative CNG channels may contribute to the tonic control of resting MVNn discharge. 8-Br-cAMP (1 mM) also elicited excitatory effects in MVNn (+40.8%), which occluded those induced by 8-Br-cGMP, indicating that the two nucleotides share a common target. Finally, nested-polymerase chain reaction assay revealed the expression of CNG channel alpha subunit transcript in MVNn. Our data provide the first demonstration that NO/cGMP signalling modulates MVNn spontaneous firing through a mechanism that is independent of PKG or PKA and probably involves activation of CNG channels.

Action Potentials↗
PubMed2007

Spatial symmetries in vestibular projections to the uvula-nodulus.

The discharge of secondary vestibular neurons relays the activity of the vestibular endorgans, occasioned by movements in three-dimensional physical space. At a slightly higher level of analysis, the discharge of each secondary vestibular neuron participates in a multifiber projection or pathway from primary afferents via the secondary neurons to another neuronal population. The logical organization of this projection determines whether characteristics of physical space are retained or lost. The logical structure of physical space is standardly expressed in terms of the mathematics of group theory. The logical organization of a projection can be compared to that of physical space by evaluating its symmetry group. The direct projection from the semicircular canal nerves via the vestibular nuclei to neck motor neurons has a full three-dimensional symmetry group, allowing it to maintain a three-dimensional coordinate frame. However, a projection may embed only a subgroup of the symmetry group of physical space, which incompletely mirrors the properties of physical space. The major visual and vestibular projections in the rabbit via the inferior olive to the uvula-nodulus carry three degrees of freedom-rotations about one vertical and two horizontal axes-but do not have full three dimensional symmetry. Instead, the vestibulo-olivo-nodular projection has symmetries corresponding to a product of two-dimensional vestibular and one-dimensional optokinetic spaces. This combination of projection symmetries provides the foundation for distinguishing horizontal from vertical rotations within a three dimensional space. In this study, we evaluate the symmetry group given by the physiological organization of the vestibulo-olivo-nodular projection. Although it acts on the same sets of elements and mirrors the rotations that occur in physical space, the physiological transformation group is distinct from the spatial group. We identify symmetries as products of physiological and spatial transformations. The symmetry group shapes the information the projection conveys to the uvula-nodulus; this shaping may depend on a physiological choice of generators, in the same way that function depends on the physiological choice of coordinates. We discuss the implications of the symmetry group for uvula-nodulus function, evolution, and functions of the vestibular system in general.

Animals↗
PubMed1992

Comparison of the effects of ACTH-(4-10) on medial vestibular nucleus neurons in brainstem slices from labyrinthine-intact and compensated guinea pigs.

The effects of adrenocorticotrophic hormone fragment 4-10 (ACTH-(4-10)) on single medial vestibular nucleus (MVN) neurons, in brainstem slices from guinea pigs which had undergone vestibular compensation for a previous ipsilateral surgical unilateral labyrinthectomy, were compared with those on MVN neurons in slices from labyrinthine-intact guinea pigs observed in a previous study. Although the average resting discharge of MVN neurons in slices from compensated animals was significantly higher than that for MVN neurons from labyrinthine-intact animals, the responses of the two groups of MVN neurons to ACTH-(4-10) were very similar. These results suggest that ACTH-(4-10) treatment is unlikely to accelerate behavioral recovery following unilateral labyrinthectomy (vestibular compensation) by acting on a receptor within the MVN for which sensitivity to ACTH-(4-10) changes during the compensation process.

Adrenocorticotropic Hormone↗
PubMed1996

Postnatal development of spontaneous tonic activity in mouse medial vestibular nucleus neurones.

The timecourse of the appearance and maturation of intrinsic tonic activity in medial vestibular nucleus (MVN) neurones was examined using extracellular single unit recording techniques in slices of the dorsal brainstem prepared from balb/c mice at specific stages during the first postnatal month. In slices from animals at postnatal day 5 (P5), the intrinsic spontaneous discharge rate was low (< 5 impulses/s on average). Over the period P10 to P30 this gradually increased to levels comparable to those of adult MVN cells in vitro. There was a rostro-caudal gradient in the time-course of development of tonic activity, such that cells located rostrally within the MVN developed higher frequencies of tonic discharge earlier than caudally located cells. The opening of the eyes around P14 was associated with a significant increase in the mean discharge rate of caudally located, but not rostrally located, MVN cells.

Age Factors↗
PubMed1996

Changes in sensitivity of vestibular nucleus neurons induced by cross-axis adaptation of the vestibulo-ocular reflex in the cat.

In alert, chronically-prepared cats, we studied response characteristics of well-isolated vestibular nucleus neurons (n = 9) while pairing yaw rotation with a pitch optokinetic stimulus, resulting in cross-axis adaptation of the horizontal vestibulo-ocular reflex. Each neuron's sensitivity to whole body rotation in a variety of axes in three-dimensional space was determined. When tested in darkness following adaptation, neurons showed statistically significant increases in sensitivity to yaw but not vertical plane rotations, suggesting participation in reflex plasticity.

Animals↗
PubMed1996

Size-related properties of vestibular afferent fibers in the frog: differential synaptic activation of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors.

Vestibular afferent fibers exhibit a specific, cell size-related uptake of aspartate and glycine [Straka H. et al. (1995) Neuroscience 70, 685-696]. A similar, size-related coexistence of glycine and glutamate had been reported earlier for these fibers [Reichenberger I. and Dieringer N. (1994) J. comp. Neurol. 349, 603-614]. Taken together, these results suggest a size-related co-release of both amino acids and the activation of different glutamate receptors in second order vestibular neurons. To test this hypothesis we stimulated the VIIIth nerve and recorded the responses of central vestibular neurons in the isolated brainstem of frogs before and during the application of the N-methyl-D-aspartate antagonists (7-chlorokynurenic acid and D-(-)-2-amino-5-phosphonovaleric acid). The presence of either one of these antagonists provoked a dose-dependent and Mg(2+)-sensitive partial block of the monosynaptic responses recorded extra- or intracellularly. This implies that afferent-evoked responses in central vestibular neurons are composed of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated components. In most of the intracellularly recorded neurons (21 out of 24) the relative amplitude of the N-methyl-D-aspartate receptor-mediated component decreased with an increase in stimulus intensity. Since electric stimulation recruits thick afferents at a lower current intensity than thin afferent fibers, our results imply a co-activation of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors by thick vestibular afferents. At a given stimulus intensity the amplitude of the N-methyl-D-aspartate receptor-mediated component differed between neurons. The results of this study extend the list of known anatomical, histochemical and physiological properties that distinguish thick from thinner vestibular afferent fibers. In spite of this detailed knowledge, however, the physiological role of thick vestibular afferents is so far unclear. The novel concept of a size-related co-activation of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors by vestibular afferent fibers establishes the basis for more specific physiological hypotheses.

2-Amino-5-phosphonovalerate↗
PubMed2000

Expansion of afferent vestibular signals after the section of one of the vestibular nerve branches.

The anterior branch of N. VIII was sectioned in adult frogs. Two months later the brain was isolated to record in vitro responses in the vestibular nuclei and from the abducens nerves following electric stimulation of the anterior branch of N. VIII or of the posterior canal nerve. Extra- and intracellularly recorded responses from the intact and operated side were compared with responses from controls. Major changes were detected on the operated side: the amplitudes of posterior canal nerve evoked field potentials were enlarged, the number of vestibular neurons with a monosynaptic input from the posterior canal nerve had increased, and posterior canal nerve stimulation recruited stronger abducens nerve responses on the intact side than vice versa. Changes in the convergence pattern of vestibular nerve afferent inputs on the operated side strongly suggest the expansion of posterior canal-related afferent inputs onto part of those vestibular neurons that were deprived of their afferent vestibular input. As a mechanism we suggest reactive synaptogenesis between intact posterior canal afferent fibers and vestibularly deprived second-order vestibular neurons.

Abducens Nerve↗
PubMed2004

Vertical eye movement-related type II neurons with downward on-directions in the vestibular nucleus in alert cats.

The vestibular nuclei and the interstitial nucleus of Cajal (INC) have been regarded as key elements of the velocity-to-position integrator for vertical eye movements. This paper reports a class of type II vestibular neurons that receives input from the INC and carries vertical eye movement signals that appear to represent an intermediate stage of the integration process. Extracellular recordings were made from neurons in and near the vestibular nuclei in alert cats. We encountered 39 neurons that exhibited an intense burst of spikes for downward saccades and a position-related tonic activity during intersaccadic intervals (d-type II neurons). They had a very high saccadic sensitivity (4.3+/-2.7 spikes/deg, mean +/- SD) as well as a high position sensitivity (3.2+/-1.6 (spikes/sec)/deg). Unlike the bursts of motoneurons, the bursts of these neurons declined gradually with an exponential-like time course and lasted well beyond the end of saccades. The mean time constant of the burst decay was 139+/-43 ms. The d-type II neurons were excited with disynaptic or trisynaptic latencies following stimulation of the contralateral vestibular nerve. The responses to vertical head rotations suggested inputs from the contralateral posterior canal. The d-type II neurons were excited with short latencies following stimulation of the ipsilateral INC, suggesting that they receive a direct excitatory input from vertical eye movement-related INC neurons with downward on-directions. The d-type II neurons were located in the rostral portion of the vestibular nuclei and the underlying reticular formation. These results suggest that d-type II neurons may be interposed between the burst-tonic neurons in the INC and pure tonic neurons in the vestibular nuclei and contribute to the oculomotor velocity-to-position integration.

Action Potentials↗
PubMedDate not supplied

The effects of steroids on vestibular compensation and vestibular nucleus neuronal activity in the guinea pig.

Recent studies have suggested that steroids such as dexamethasone and methylprednisolone might be useful in the treatment of vestibular disorders, irrespective of whether inflammatory processes are involved. The aim of this study was to investigate the effects of systemic administration of dexamethasone on vestibular compensation of spontaneous nystagmus (SN) in guinea pig, and the effects of dexamethasone and methylprednisolone on extracellularly recorded spontaneous activity of medial vestibular nucleus (MVN) neurons in brainstem slices in vitro. In the behavioral study, none of the 3 doses of dexamethasone (5, 10, or 40 mg/kg i.p., delivered at 0, 12, 24, and 36 h following a unilateral surgical labyrinthectomy (UL)) resulted in a significant change in the frequency or compensation of SN, relative to the vehicle control group. In the in vitro study, only a minority of MVN neurons showed any response to 1 microM dexamethasone (1 out of 9 neurons), or 10 nM (3 out of 13), or 0.1 microM methylprednisolone (3 out of 7). These results suggest, contrary to previous evidence, that dexamethasone may not accelerate compensation of SN following surgical UL and that dexamethasone and methylprednisolone may have a direct action only on a minority of MVN neurons.

Action Potentials↗
PubMed1982

Responses of afferent and efferent neurons to visual inputs in the vestibular nerve of the frog.

In the frog immobilized by intralymphatic injection of D-tubocurarine, stimulation of the visual apparatus with either electrical shocks applied to the optic chiasma or light pulses elicited, in many cases, an increase and a decrease of firing of efferent and afferent vestibular neurons, respectively, recorded from the horizontal semicircular canal nerve. Optokinetic stimulation was completely inefficient in modulating the efferent and afferent discharge. These results show that stimulation of the visual system can modify vestibular apparatus fuctioning at the most peripheral level. However, it is likely that the effects observed were due to an arousal phenomenon or/and to a motor corollary discharge.

Action Potentials↗
PubMed1991

[Impulse activity of neurons of the lateral vestibular nucleus in guinea pigs during locomotion].

The influence of spontaneous locomotion on the resting impulse activity of the lateral vestibular nucleus neurons was investigated in the decerebrated guinea pig. Appearance of the rhythmic limb muscle activity was followed by an increase of the frequency of the resting discharge from 10-50 to 100 imp./s. An increase in the frequency of discharges was observed at the beginning of the forelimb extensor muscle activity, i.e. at the end of the swing phase and beginning of the stance phase of the locomotor cycle. It is suggested that the observed changes in the activity of vestibular neurons provide high tonus of antigravitational muscles, which is the base for rhythmic movements of the limbs.

Animals↗
PubMed1992

Direct muscarinic and nicotinic receptor-mediated excitation of rat medial vestibular nucleus neurons in vitro.

We have utilized intracellular recording techniques to investigate the cholinoceptivity of rat medial vestibular nucleus (MVN) neurons in a submerged brain slice preparation. Exogenous application of the mixed cholinergic agonists, acetylcholine (ACh) or carbachol (CCh), produced predominantly membrane depolarization, induction of action potential firing, and decreased input resistance. Application of the selective muscarinic receptor agonist muscarine (MUSC), or the selective nicotinic receptor agonists nicotine (NIC) or 1,1-dimethyl-4-phenylpiperazinium (DMPP) also produced membrane depolarizations. The MUSC-induced depolarization was accompanied by decreased conductance, while an increase in conductance appeared to underlie the NIC- and DMPP-induced depolarizations. The muscarinic and nicotinic receptor mediated depolarizations persisted in tetrodotoxin and/or low Ca2+/high Mg2+ containing media, suggesting direct postsynaptic receptor activation. The MUSC-induced depolarization could be reversibly blocked by the selective muscarinic-receptor antagonist, atropine, while the DMPP-induced depolarization could be reversibly suppressed by the selective ganglionic nicotinic-receptor antagonist, mecamylamine. Some neurons exhibited a transient membrane hyperpolarization during the depolarizing response to CCh or MUSC application. This transient inhibition could be reversibly blocked by the gamma-aminobutyric acid (GABA) antagonist, bicuculline, suggesting that the underlying hyperpolarization results indirectly from the endogenous release of GABA acting at GABA receptors. This study confirms the cholinoceptivity of MVN neurons and establishes that individual MVN cells possess muscarinic as well as nicotinic receptors. The data provide support for a prominent role of cholinergic mechanisms in the direct and indirect regulation of the excitability of MVN neurons.

Animals↗