VESTIBULAR AND MUSCLE NERVE CONNECTIONS TO PYRAMIDAL TRACT NEURONS OF CAT.
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Asphyxia↗
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Extracellular recording of vestibulo-thalamic neurons projecting to the spinal cord in the cat.
Forty vestibulo-thalamic (VT) neurons were recorded extracellularly in the vestibular nuclei of the anesthetized cat. More than half of the VT neurons responded monosynaptically to vestibular nerve stimulation; the others responded polysynaptically. The VT neurons were activated antidromically from one or two sites in the contralateral VPL, VPM, VL, VM, SG, and PO in the thalamus. Their axonal arborizations in the thalamus were likely restricted in narrow areas. About three quarters of the VT neurons were also activated antidromically from the ventral funiculus in the C1 segment. Axonal branchings were found in the contralateral C1 gray matter. The VT neurons were mainly localized in the descending vestibular nucleus.
Animals↗
Differential regulation of GABA(A) and GABA(B) receptors during vestibular compensation.
We investigated changes in intrinsic excitability and GABA receptor efficacy in rat medial vestibular nucleus (MVN) neurons following 48 h and 7-10 days of behavioral recovery after unilateral labyrinthectomy (UL) in the rat. The mean in vitro discharge rate of rostral ipsilesional MVN cells at both time points was significantly higher than normal, indicating that the intrinsic excitability of the deafferented cells undergoes a sustained up-regulation during vestibular compensation. In slices from animals that had compensated for 7-10 days after UL, the responsiveness of rostral ipsilesional MVN cells to the GABA(A) agonist muscimol was not different from normal, while the responsiveness to the GABA(B) agonist baclofen was significantly down-regulated. This is in contrast to the situation soon after UL, where the efficacy of both GABA(A) and GABA(B) receptors is markedly down-regulated. The recovery of fast GABA(A) mediated neurotransmission by 7-10 days post-UL presumably enables ipsilesional cells to again respond to vestibular stimulation, through commissural inhibitory modulation from the intact side. The permanent loss of excitatory input from the lesioned side may be, in effect, counteracted by the long-term down-regulation of slow GABA(B) receptors in the de-afferented neurons.
Adaptation, Physiological↗
Localization and origins of calcitonin gene-related peptide containing fibres in the vestibular end-organs of the rat.
The distribution, origin and fine structure of nerve terminals immunoreactive to calcitonin gene-related peptide (CGRP) were investigated in the vestibular end-organs of the rat by means of immunocytochemistry. Dense plexus of CGRP-like immunoreactive (CGRPI) fibres were observed just beneath the sensory epithelial layers of the ampullary crista of the semicircular canal, and utricular and saccular maculae of the otolith organ. Some CGRPI fibres left the plexus to enter the sensory epithelial layer. Parasagittal transection of the brain just medial to the cochlear nucleus revealed the presence of a few CGPRI fibres in the vestibular end-organs ipsilaterally, indicating that these fibres originate in the central nervous system. A combination of retrograde tracing and immunocytochemistry was then used to identify the origins of CGRPI fibres found in the vestibular end-organs. After injection of fast blue dye (FB) into the vestibular cistern, CGRPI neurons in the area dorsolateral to the genu of the facial nerve were labelled by FB bilaterally. The present ultrastructural study has revealed that most of the CGRPI fibres in the vestibular end-organs form direct contacts with afferent nerve terminals which surround type I vestibular sensory cells.
Acoustic Maculae↗
Short-term vestibulo-ocular reflex adaptation in humans. II. Error signals.
We oscillated humans sinusoidally at 0.2 Hz for 1 h, using various combinations of rotations of the head and visual surround to elicit short-term adaptation of the gain of the vestibulo-ocular reflex (VOR). Before and after each period of training, the gain of the VOR was measured in darkness, in response to a position step of head rotation. A small foveal target served as well as a full-field stimulus at driving VOR adaptation. Oscillation of the visual surround alone produced a substantial increase in the VOR gain. When the visual scene was rotated in phase with the head but with a larger amplitude to produce a reversal of the VOR, the VOR gain increased if the movement of the visual scene was much greater than that of the head, otherwise the gain decreased. We interpreted these results with a model of VOR adaptation that uses as its "error signal" the combination of motion of images on the retina (retinal slip) and any additional slow-phase eye velocity, beyond that generated by the VOR through the vestibular nuclei, necessary to prevent such retinal slip during head rotation. The slow phase velocity generated by the VOR is derived from "inferred head rotation", a signal based on the discharge of neurons in the vestibular nuclei that receive both labyrinthine and visual (optokinetic) inputs. The amplitude and sign of the ratio of the "error signal" to "inferred head velocity" determined the amplitude and the direction (increase or decrease) of VOR gain adaptation.
Adaptation, Physiological↗
Adaptive changes in vergence eye movements induced by vergence-vestibular interaction training in monkeys.
Clear vision of objects moving in three-dimensional space near an observer is attained by a combination of smooth-pursuit and vergence eye movements. The two systems must interact with the vestibular system to maintain the image of the object on the fovea. Previous studies showed that training with smooth-pursuit vestibular interactions resulted in adaptive changes in the smooth-pursuit response. Although vergence and smooth-pursuit systems are thought to have separate neural substrates, recent studies indicate that the caudal parts of the frontal eye fields that receive vestibular inputs contain neurons that discharge in response to combinations of smooth-pursuit and vergence. This combination of discharge sensitivities suggests the possibility that adaptive changes may be induced in the vergence system by vestibular inputs during vergence-pursuit training. To explore this possibility, we examined the effects of training with conflicting vestibular and vergence tracking in four head-stabilized monkeys. Animals were rewarded for tracking a laser spot that moved towards or away from them at 1 Hz in phase with sinusoidal whole-body rotation (+/- 5 degrees) in the pitch plane; the spot moved closer when the monkey's nose moved downward. From the monkey's point of view, the spot moved sinusoidally 10-66 cm in front of them along the mid-sagittal plane, requiring symmetrical vergence eye movements of 4.8 degrees for each eye. Eye movements induced by equivalent spot motion at 0.3-1.0 Hz with or without chair rotation were examined before and after training for each session (0.5-1.0 h). Before training, pitch rotation alone in complete darkness did not induce vergence eye movements in any of the monkeys tested. Vergence tracking without chair rotation showed decreased gain and increased phase lag (re vergence target velocity) at frequencies above 0.5 Hz. After training, the vergence response during chair rotation with the spot showed significantly higher gains and smaller phase lags at 0.3-1.0 Hz in all monkeys. Pitch rotation alone in complete darkness induced vergence eye movements with gains (eye vergence/chair) of 0.15-0.35 after training in two monkeys. These results suggest that vestibular information can be used effectively to modify vergence tracking.
Adaptation, Physiological↗
[Behavior of the motor neurons of the external oculomotor nucleus during vestibular stimulation in the waking cat].
The electrical activity of abducens motoneurons during sinusoidal stimulation of the head has been recorded in alert cats. Recorded motoneurons were identified by their antidromic activation from the VIth nerve. The profile of motoneuronal firing rate showed a sinusoidal modulation leading eye position in the orbit. Motoneuron firing rate was decomposed in two separate components, proportional and in phase with eye position (k) and velocity (r), respectively. Time constant of each motoneuron, calculated from phase lead analysis, was similar to that calculated from k and r coefficients. Functional implications of described findings are discussed.
Abducens Nerve↗
Responses of feline medial medullary reticular formation neurons with projections to the C5-C6 ventral horn to vestibular stimulation.
Prior studies have shown that the vestibular system contributes to adjusting respiratory muscle activity during changes in posture, and have suggested that portions of the medial medullary reticular formation (MRF) participate in generating vestibulo-respiratory responses. However, there was previously no direct evidence to demonstrate that cells in the MRF relay vestibular signals monosynaptically to respiratory motoneurons. The present study tested the hypothesis that the firing of MRF neurons whose axons could be antidromically activated from the vicinity of diaphragm motoneurons was modulated by whole-body rotations in vertical planes that stimulated vestibular receptors, as well as by electrical current pulses delivered to the vestibular nerve. In total, 171 MRF neurons that projected to the C5-C6 ventral horn were studied; they had a conduction velocity of 34+/-15 (standard deviation) m/sec. Most (135/171 or 79%) of these MRF neurons lacked spontaneous firing. Of the subpopulation of units with spontaneous discharges, only 3 of 20 cells responded to vertical rotations up to 10 degrees in amplitude, whereas the activity of 8 of 14 neurons was affected by electrical stimulation of the vestibular nerve. These data support the hypothesis that the MRF participates in generating vestibulo-respiratory responses, but also suggest that some neurons in this region have other functions.
Analysis of Variance↗
Perineuronal nets provide a polyanionic, glia-associated form of microenvironment around certain neurons in many parts of the rat brain.
The nature and function of previously described perineuronal nets are still obscure. In the present study their polyanionic components were demonstrated in the rat brain using colloidal iron hydroxide (CIH) staining. In subcortical regions, such as the red nucleus, cerebellar, and vestibular nuclei, most neurons were ensheathed by CIH-binding material. In the cerebral cortex perineuronal nets were seen around numerous nonpyramidal neurons. Biotinylated hyaluronectin revealed that hyaluronan occurs in perineuronal nets. Two plant lectins [Wisteria floribunda agglutinin (WFA) and Vicia villosa agglutinin (VVA)] with affinity for N-acetylgalactosamine visualized perineuronal nets similar to those rich in anionic components. Glutamic acid decarboxylase (GAD)-immunoreactive synaptic boutons were shown to occupy numerous meshes of perineuronal VVA-positive nets. Electron microscopically, VVA binding sites were scattered throughout perisynaptic profiles, but accumulated at membranes and in the extracellular space except not in synaptic clefts. To investigate the spatial relationship between glial cell processes and perineuronal nets, two astrocytic markers (S100-protein and glutamine synthetase) were visualized at the light and electron microscopic level. Two methods to detect microglia by the use of Griffonia simplicifolia agglutinin (GSA I-B4) and the monoclonal antibody, OX-42, were also applied. Labelled structures forming perineuronal nets were observed with both astrocytic, but not with microglial, markers. It is concluded that perineuronal nets are composed of a specialized type of glia-associated extracellular matrix rich in polyanionic groups and N-acetylgalactosamine. The net-like appearance is due to perisynaptic arrangement of the astrocytic processes and these extracellular components. Similar to the ensheathment of nodes of Ranvier, perineuronal nets may provide a special ion buffering capacity required around various, perhaps highly active, types of neurons.
Acetylgalactosamine↗
Postsynaptic targets of Purkinje cell terminals in the cerebellar and vestibular nuclei of the rat.
The cerebellar and vestibular nuclei consist of a heterogeneous group of inhibitory and excitatory neurons. A major proportion of the inhibitory neurons provides a GABAergic feedback to the inferior olive, while the excitatory neurons exert more direct effects on motor control via non-olivary structures. At present is is not clear whether Purkinje cells innervate all types of neurons in the cerebellar and vestibular nuclei or whether an individual Purkinje cell axon can innervate different types of neurons. In the present study, we studied the postsynaptic targets of Purkinje cell axons in the rat using a combination of pre-embedding immunolabelling of the Purkinje cell terminals by L7, a Purkinje cell-specific marker, and postembedding GABA and glycine immunocytochemistry. In the cerebellar nuclei, vestibular nuclei and nucleus prepositus hypoglossi Purkinje cell terminals were found apposed to GABAergic and glycinergic neurons as well as to larger non-GABAergic, non-glycinergic neurons. In the cerebellar and vestibular nuclei individual Purkinje cell terminals innervated both the inhibitory and excitatory neurons. Both types of neurons were contacted no only by non-GABAergic Purkinje cell terminals but also by GABA-containing terminals that were not labelled for L7 and by non-GABAergic, non-glycinergic terminals that formed excitatory synapses. Glycine-containing terminals were relatively scarce ( < 2% of the GABA-containing terminals) and frequently contacted the larger non-GABAergic, non-glycinergic neurons. To summarize, Purkinje cell axons evoke their effects through different types of neurons present in the cerebellar and vestibular nuclear complex. The observation that individual Purkinje cells can innervate both excitatory and inhibitory neurons suggests that the excitatory cerebellar output system and the inhibitory feedback to the inferior olive are controlled simultaneously.
Afferent Pathways↗
Development of the ear and of connections between the ear and the brain: is there a role for gravity?
This paper outlines the development of the gravistatic sensory system of the ear. First, evidence is presented that a genetic program, for which major transcription factors have already been identified using gene expression studies and targeted mutagenesis, governs the initial development of this system. Second, the formation of sensory neurons and their connections to the brain is described as revealed by tracing studies and genetic manipulations. It is concluded that the initial development of the connections of sensory neurons with mechanosensory transducers of the ear (the hair cells) and the targets in the brainstem (vestibular nuclei) is also dependent on fairly rigid genetic programs. During late embryonic and early postnatal development, however, sensory input appears to be used to fine-tune connections of these sensory neurons with the hair cells in the ear as well as with second order vestibular neurons in the brainstem. This phase is proposed to be critical for a proper calibration of the gravistatic information processing in the brain.
Animals↗
The control of posture and movements during REM sleep: neurophysiological and neurochemical mechanisms.
Mammalian sleep is characterized by synchronized sleep, in which high-amplitude, low-frequency waves appear in the electroencephalogram, and desynchronized sleep, characterized by small-amplitude, high-frequency waves, absence of tonic muscle activity, and rapid eye movements (REM), which are associated in humans with dreams. The postural atonia typical of desynchronized sleep is due to postsynaptic inhibition of spinal motoneurons resulting from tonic activation of a bulbospinal inhibitory system. Superimposed on this background of postural atonia, a motor pattern appears, characterized by rapid contractions of the limb musculature synchronous with the REM bursts. Simultaneously one observes phasic inhibition of transmission of somatic afferent volleys to motoneurons and ascending spinal pathways. The bursts of REM depend upon rhythmic discharges of vestibulo-oculomotor neurons, due to extralabyrinthine volleys originating from the brainstem. Ascending and descending vestibular volleys are also able to excite corticospinal and other supraspinal descending neurons responsible for the motor events synchronous with the bursts of REM. Activation of cholinergic neurons located in the brainstem reticular formation reproduces the postural atonia typical of desynchronized sleep, as well as the phasic events characterized by the REM bursts and the related changes in spinal cord activities. Even in this instance the bursts of REM and the related spinal effects depend upon rhythmic changes in the discharge of vestibular nuclear neurons. Experimental evidence indicates that the cholinergic reticular neurons fire asynchronously, thus being able to trigger the bulbospinal inhibitory system responsible for postural atonia. Even the vestibulo-oculomotor neurons are activated by these cholinergic reticular neurons; however, the continuous stream of these extralabyrinthine impulses is transformed into rhythmic changes of discharge of the vestibular nuclear neurons due to the presence of inhibitory neurons interposed with the vestibulo-oculomotor system. Waxing and waning in the activity of these cholinergic reticular neurons accounts for the regular occurrence of the cholinergically induced bursts of REM.
Adrenergic Uptake Inhibitors↗
A quantitative study of the vestibular commissures in the gerbil.
Direct commissural connections between the bilateral vestibular nuclear complexes (VNC) were investigated in the gerbil using ionophoretic injections of horseradish peroxidase into individual vestibular nuclei. Labelled commissural neurons were counted, the cell counts adjusted by the relative nuclear volume, and the results treated quantitatively. The medial nucleus (MVN) contained the greatest number of commissural neurons. The MVN projected to each of the contralateral vestibular nuclei, but most strongly to the contralateral MVN and superior (SVN) nucleus. The SVN projected modestly to the contralateral VNC. Commissural connections of the descending nucleus were weak. Commissural afferents to the MVN were topographically organized. The crossed fastigiovestibular projection was also investigated.
Animals↗
Autoantibodies to glutamic acid decarboxylase in downbeat nystagmus.
The cause of downbeat nystagmus (DBN) remains undiagnosed in about 40% of patients. This paper reports the presence of antiglutamic acid decarboxylase antibodies (GAD-Ab) in a patient with DBN. Antibodies against GABAergic neurons located in the vestibular complex may induce chemical denervation of the floccular neurons, which normally suppress the peripheral imbalance between vertical semicircular canal systems, thereby causing DBN. Testing for GAD-Ab may be indicated in DBN patients without an identifiable anatomical brain lesion.
Aged↗
Neural basis for motor learning in the vestibuloocular reflex of primates. III. Computational and behavioral analysis of the sites of learning.
1. We have used a combination of eye movement recordings and computer modeling to study long-term adaptive modification (motor learning) in the vestibuloocular reflex (VOR). The eye movement recordings place constraints on possible sites for motor learning. The computer model abides by these constraints, as well as constraints provided by data in previous papers, to formalize a new hypothesis about the sites of motor learning. The model was designed to reproduce as much of the existing neural and behavioral data as possible. 2. Motor learning was induced in monkeys by fitting them with spectacles that caused the gain of the VOR (eye speed divided by head speed) to increase to values > 1.6 or to decrease to values < 0.4. We elicited pursuit by providing ramp motion of a small target at 30 degrees/s along the horizontal axis. Changes in the gain of the VOR caused only small and inconsistent changes in the eye acceleration in the first 100 ms after the onset of pursuit and had no effect on the eye velocity during tracking of steady target motion. Electrical stimulation in the flocculus and ventral paraflocculus with single pulses or trains of pulses caused smooth eye movement toward the side of stimulation after latencies of 9-11 ms. Neither the latency, the peak eye velocity, nor the initial eye acceleration varied as a consistent function of the gain of the VOR. 3. The computer model contained nodes that represented position-vestibular-pause cells (PVP-cells) and flocculus target neurons (FTNs) in the vestibular nucleus, and horizontal gaze-velocity Purkinje cells (HGVP-cells) in the cerebellar flocculus and ventral paraflocculus. Node FTN represented only the "E-c FTNs," which show increased firing for eye motion away from the side of recording. The transfer functions in the model included dynamic elements (filters) as well as static elements (summing junctions, gain elements, and time delays). Except for the transfer functions that converted visual motion inputs into commands for smooth eye movement, the model was linear. 4. The performance of the model was determined both by computer simulation and, for the VOR in the dark, by analytic solution of linear equations. For simulation, we adjusted the parameters by hand to match the output of the model to the eye velocity of monkeys and to match the activity of the relevant nodes in the model to the firing of HGVP-cells, FTNs, and PVP-cells when the gain of the VOR was 0.4, 1.0, and 1.6.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Spatio-temporal diversity in the microenvironments for neural cell adhesion molecule, neural cell adhesion molecule-polysialic acid, and L1-cell adhesion molecule expression by sensory neurons and their targets during cochleo-vestibular innervation.
Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell adhesion molecules, neural cell adhesion molecule, neural cell adhesion molecule-polysialic acid, and L1-cell adhesion molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell adhesion molecule, but not L1-cell adhesion molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell adhesion molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell adhesion molecule, but not L1-cell adhesion molecule. Post-migratory ganglion cell processes expressed both molecules in all stages. The cell adhesion molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell adhesion molecule expression followed the innervation gradient. Neural cell adhesion molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell adhesion molecule, but not L1-cell adhesion molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell adhesion molecule, but not neural cell adhesion molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell adhesion molecules in the floorplate. Commissural axons expressed both cell adhesion molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell adhesion molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the molecules critical for the changing roles of the microenvironment in neuronal specification.
Animals↗
Cellular and subcellular localization of AMPA-selective glutamate receptors in the mammalian peripheral vestibular system.
The cellular and subcellular distribution of AMPA-selective glutamate receptors in the mammalian peripheral vestibular system was examined using antibodies against peptides corresponding to the C-terminal portions of AMPA receptor subunits: GluR1, GluR2/R3 and GluR4. The light and electron microscopic immunocytochemical studies were carried out on Vibratome sections of rat and guinea pig vestibular sensory epithelial and ganglia. In the epithelium, GluR1 subunit immunoreactivity appeared as accumulations of patches outlining the baso-lateral periphery of the type I sensory cells. The GluR1-immunoreactive microareas were postsynaptically distributed on the membranes of calyceal afferent fibers. GluR2/R3 immunoreactivity was present in the sensory cells. GluR4 was not detected. In the vestibular ganglion, the neurons were densely stained with antibodies to GluR2/R3 and GluR4. The fibroblasts and the Schwann cells were also intensely stained with antibodies to GluR2/R3 and GluR4. In the sensory cells, the AMPA receptors, GluR2/R3, may function as (1) autoreceptors controlling afferent neurotransmitter release or (2) 'postsynaptic' receptors activated by the neurotransmitter release of the afferent calyx. The detection of GluR1 at postsynaptic sites in the afferent fibers provides anatomical evidence for the role of glutamate as a neurotransmitter of sensory cells. In the ganglion neurons, GluR2/R3 and GluR4 may represent reserve intracytoplasmic pools of receptor subunits in transit to the postsynaptic sites. In the Schwann cells, GluR2/R3 and GluR4 may be involved in neuronal-glial signalling at the nodes of Ranvier.
Animals↗
GABAA receptor-like immunoreactivity in the goldfish brainstem with emphasis on the Mauthner cell.
The distribution of the GABAA receptor in the goldfish brainstem and on the Mauthner cell membrane was investigated with both optical and electron microscopy using a polyclonal antibody raised against the intracellular loop of the rat gamma 2 subunit. At the optical level, immunofluorescent dots were detected on small and large neurons belonging to vestibular and reticular nuclei. On the Mauthner cell plasmalemma, a gamma 2-like immunoreactivity was observed predominantly on the tip of the lateral dendrite. Fluorescent parches were intermingled with a more diffuse staining. Immunoreactive spots of weaker intensity were also present on the soma and some were also observed inside and within the periphery of the axon-cap as well. Observations at the electron microscopic level revealed that the peroxidase end-product predominates postsynaptically in front of release sites in the studied nuclei and on the Mauthner cell. On the lateral dendrite of the neuron, numerous immunopositive postsynaptic differentiations were encountered on spines. Stained glial elements were encountered in the different areas studied. These results demonstrate that the GABAA receptor gamma 2 subunit has a precise distribution on neuronal membranes and suggest that it could be involved in the remote dendritic inhibition of the Mauthner cell and in the control of input-output properties of both vestibular and reticular nuclei.
Animals↗