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PubMed1993

Distribution of the inositol 1,4,5-trisphosphate receptor, P400, in adult rat brain.

The distribution of the inositol 1,4,5-trisphosphate receptor protein, P400, was investigated in adult rat brain by immunocytochemistry with the monoclonal antibody 4C11 raised against mouse cerebellar inositol 1,4,5-trisphosphate receptor protein. Immunoreactive neuronal cell bodies were detected in the cerebral cortex, the claustrum, the endopiriform nucleus, the corpus callosum, the anterior olfactory nuclei, the olfactory tubercle, the nucleus accumbens, the lateral septum, the bed nucleus of the stria terminalis, the hippocampal formation, the dentate gyrus, the caudate-putamen, the fundus striatum, the amygdaloid complex, the thalamus, the caudolateral part of the hypothalamus, the supramammillary nuclei, the substantia nigra, the pedunculopontine tegmental nucleus, the ventrotegmental area, the Purkinje cells in the cerebellum, the dorsal cochlear nucleus, the subnucleus oralis and caudalis of trigeminal nerve, and the dorsal horn of the spinal cord. Immunoreactive fibres were found in the medial forebrain bundle, the globus pallidus, the stria terminalis, the pyramidal tract, the spinal tract of trigeminal nerve, and the ventral horn of spinal cord. Nerve fibres forming a dense plexus ending in terminal-like boutons were detected in relation to nonimmunoreactive neurons of the dentate, interpositus, and fastigial nuclei of the cerebellum and around neurons of the vestibular nuclei. This receptor protein binds a specific second messenger, inositol 1,4,5-trisphosphate, which produces a mobilization of intracellular Ca2+ and a modulation of transmitter release.

Animals↗
PubMed1999

trkA, trkB, and trkC messenger RNA expression by bulbospinal cells of the rat.

Previous research has shown that corticospinal as well as rubrospinal neurons express the high-affinity trkB and trkC receptors but not the high-affinity trkA receptor. To determine if bulbospinal neurons in other brainstem areas show the same pattern of trk receptor expression, bulbospinal cells were labelled via the injection of the retrograde tracer FluoroGold into the spinal cord. Brainstem sections were then processed for in situ hybridization using oligonucleotide probes to the trkA, trkB, and trkC receptors. The results indicated that, although trkA expression occurred in brainstem areas that contain bulbospinal neurons (e.g., the vestibular nuclei, and the pontine reticular formation), very few FluoroGold-labelled cells expressed the trkA receptor. In contrast, at least 90% of bulbospinal cells in each brainstem area examined expressed the trkB receptor. Quantitative analysis indicated differences in the level of trkB labelling between bulbospinal cells in different brainstem areas, with the highest levels seen in the locus coeruleus and magnocellular portion of the red nucleus, and the lowest levels seen in the medial and superior vestibular nuclei and the raphe obscurus. With the exception of the accessory trigeminal nucleus, over 84% of bulbospinal cells in each brainstem area also expressed the trkC receptor. TrkC receptor expression was greatest in the locus coeruleus and subcoeruleus and lowest in the accessory trigeminal nucleus, the raphe magnus, and the vestibular nuclei. Results indicate that, as with other descending pathways, virtually all bulbospinal pathways should be amenable to treatment with brain-derived neurotrophic factor, neurotrophin-4/5 or neurotrophin-3, but not nerve growth factor, following spinal cord damage.

Animals↗
PubMed1995

Repetitive paroxysmal nystagmus and vertigo.

A 55-year-old woman had paroxysms of vertigo and visual blurring associated with complex combined torsional, horizontal, and vertical nystagmus. These episodes occurred regularly at 2-minute intervals, each attack lasting for 15 seconds. Between attacks, there was a much finer asymptomatic nystagmus whose components were in the opposite direction to those associated with the paroxysmal attacks. A brain MRI revealed an arteriovenous malformation in close proximity to the left vestibular nucleus, with evidence of previous bleeding. Caloric testing demonstrated a left-sided vestibular paresis. We suggest that neurons in this patient's damaged left vestibular nucleus are usually underactive but regularly produce pathologic brief bursts of hyperactivity causing episodic reversal and gross exacerbation of her resting nystagmus. Treatment with low-dose carbamazepine was successful in abolishing both the paroxysms of nystagmus and the symptoms of vertigo and visual disturbance.

Arteriovenous Malformations↗
PubMed1992

Pretreatment with MK-801 reduces spontaneous nystagmus following unilateral labyrinthectomy.

Unilateral labyrinthectomy results in a syndrome of ocular motor and postural symptoms which abate over time in a process of behavioural recovery known as vestibular compensation. We have previously suggested that an increased Ca2+ influx in ipsilateral vestibular nucleus (VN) neurons at the time of the unilateral labyrinthectomy may exacerbate the depression of VN resting activity caused by the loss of excitatory input from the VIIIth nerve. In order to further test this hypothesis, we administered (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801; 1.0 or 2.5 mg/kg i.p.), which blocks Ca2+ influx via NMDA receptor-mediated ion channels, to guinea pigs 0.5 h before unilateral labyrinthectomy and examined the effects on three symptoms of unilateral labyrinthectomy: spontaneous ocular nystagmus, yaw head tilt and roll head tilt. Pretreatment with MK-801 significantly altered the time course of the vestibular compensation of spontaneous nystagmus and yaw head tilt but had no significant effect on roll head tilt; in particular, 2.5 mg/kg MK-801 depressed spontaneous nystagmus frequency at 10 and 20 h post-labyrinthectomy relative to saline controls (P less than 0.05, post-hoc Scheffé F-test). The reduction in spontaneous nystagmus frequency was not simply a result of extended anesthesia, since other control animals, which received additional injections of the general anesthetic in order to achieve equivalent sleep times to the MK-801 group, did not show reduced spontaneous nystagmus frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1998

Extracellular nucleotide signaling in the inner ear.

Extracellular nucleotides, particularly adenosine 5'-triphosphate (ATP), act as signaling molecules in the inner ear. Roles as neurotransmitters, neuromodulators, and as autocrine or paracrine humoral factors are evident. The diversity of the signaling pathways for nucleotides, which include a variety of ATP-gated ion channels (assembled from different subtypes of P2X-receptor subunit) and also different subtypes of G protein-coupled nucleotide receptors (P2Y receptors) supports a major physiological role for ATP in the regulation of hearing and balance. Almost invariably both P2X and P2Y receptor expression is apparent in the complex tissue structures associated with the inner-ear labyrinth. However P2X-receptor expression, commonly associated with fast neurotransmission, is apparent not only with the cochlear and vestibular primary afferent neurons, but also appears to mediate humoral signaling via ATP-gated ion channel localization to the endolymphatic surface of the cochlear sensory epithelium (organ of Corti). This is the site of the sound-transduction process and recent data, including both electrophysiological, imaging, and immunocytochemistry, has shown that the ATP-gated ion channels are colocalized here with the mechano-electrical transduction channels of the cochlear hair cells. In contrast to this direct action of extracellular ATP on the sound-transduction process, an indirect effect is apparent via P2Y-receptor expression, prevalent on the marginal cells of the stria vascularis, a tissue that generates the standing ionic and electrical gradients across the cochlear partition. The site of generation of these gradients, including the dark-cell epithelium of the vestibular labyrinth, may be under autocrine or paracrine regulation mediated by P2Y receptors sensitive to both purines (ATP) and pyrimidines such as UTP. There is also emerging evidence that the nucleoside adenosine, formed as a breakdown product of ATP by the action of ectonucleotidases and acting via P1 receptors, is also physiologically significant in the inner ear. P1-receptor expression (including A1, A2, and A3 subtypes) appear to have roles associated with stress, acting alongside P2Y receptors to enhance cochlear blood flow and to protect against the action of free radicals and to modulate the activity of membrane conductances. Given the positioning of a diverse range of purinergic-signaling pathways within the inner ear, elevations of nucleotides and nucleosides are clearly positioned to affect hearing and balance. Recent data clearly supports endogenous ATP- and adenosine-mediated changes in sensory transduction via a regulation of the electrochemical gradients in the cochlea, alterations in the active and passive mechanical properties of the cells of the sensory epithelium, effects on primary afferent neurons, and control of the blood supply. The field now awaits conclusive evidence linking a physiologically-induced modulation of extracellular nucleotide and nucleoside levels to altered inner ear function.

Animals↗
PubMed1992

Distribution of calcitonin gene-related peptide immunoreactivity in the central nervous system of the frog, Rana esculenta.

The distribution of calcitonin gene-related peptide (CGRP), immunoreactive structures in the central nervous system of the frog, Rana esculenta, was studied using the peroxidase immunohistochemical method. Immunoreactive perikarya were found in all major parts of the brain. In the forebrain, neurons of the septohippocampal formation, the amygdala, the ventromedial and posterocentral thalamic nuclei, and the cerebrospinal fluid contacting neurons in the diencephalic periventricular organ showed immunoreactivity. The pear-shaped neurons of the optic tectum, and perikarya of the oculomotor nucleus in the midbrain were also immunoreactive. In the hindbrain, neurons of the cranial nerve motor nuclei, neurons of the superior vestibular nucleus, giant cells of the reticular formation, and preganglionic parasympathetic neurons of the superior salivatory nucleus were stained. Motoneurons presented immunostaining also in the spinal cord. Immunoreactive fibers were shown to occur in the olfactory tract, the striatum, the tegmentum and the basis mesencephali, the descending tract of the trigeminal nerve, the solitary tract, Lissauer's tract, and the dorsal horn of spinal cord. A comparison of the distribution of CGRP immunoreactivity in the mammalian and amphibian central nervous system revealed that, in relation to the size of the brain, CGRP is more extensively distributed in the amphibian than in the mammalian limbic system.

Animals↗
PubMed1995

The acoustic startle reflex: neurons and connections.

The startle reflex protects animals from blows or predatory attacks by quickly stiffening the limbs, body wall and dorsal neck in the brief time period before directed evasive or defensive action can be performed. The acoustic startle reflex in rats and cats is mediated primarily by a small cluster of giant neurons in the ventrocaudal part of the nucleus reticularis pontis caudalis (RPC) of the reticular formation. Activation of these RPC neurons occurs 3-8 ms after the acoustic stimulus reaches the ear. Undetermined neurons of the cochlear nuclei activate RPC via weak monosynaptic and strong disynaptic connections. The strong disynaptic input occurs via neurons of the contralateral ventrolateral pons, including large neurons of the ventrolateral tegmental nucleus that integrate auditory, tactile and vestibular information. RPC giant neurons, in turn, activate hundreds of motoneurons in the brain stem and the length of the spinal cord via large reticulospinal axons near the medial longitudinal fasciculus. To hindlimb motoneurons, monosynaptic connections from the reticulospinal tract are weak, but disynaptic connections via spinal cord interneurons are stronger and show temporal facilitation, like the startle response itself.

Animals↗
PubMed1993

Vestibulospinal reflexes and the reticular formation.

While both vestibulospinal and reticulospinal tracts contribute to vestibulospinal reflexes, their respective roles are not fully understood. Previous evidence suggests that reticulospinal fibers make an important contribution to the horizontal vestibulocollic reflex (VCR) of the decerebrate cat. Recent work addresses their contribution to the vertical VCR. On the basis of study of reflex and vestibulocollic neuron dynamics, it appears that processing which is necessary to produce some of the spatial properties of the vertical VCR takes place outside the vestibular nuclei. Recording from pontomedullary reticulospinal neurons receiving vestibular input and projecting to different levels of the spinal cord reveals that almost no cells receive only vertical canal input, while approximately half receive otolith input. As is the case for vestibulocollic neurons, these reticulospinal neurons also lack the properties required to produce all of the VCR's spatial properties. Two conclusions are that in response to stimuli in vertical planes pontomedullary reticulospinal fibers are best suited to contribute to otolith reflexes, and that spatial properties of the VCR depend in part on convergence of inputs within the neck itself.

Motor Neurons↗
PubMed1991

Synapsin I and Synaptophysin expression during ontogenesis of the mouse peripheral vestibular system.

Synapsin I and Synaptophysin are selectively localized in axonal endings of CNS neurons where they are associated with small synaptic vesicle membranes. The development of expression of these 2 proteins was studied by immunocytochemistry during ontogenesis of the peripheral vestibular system in the mouse. Both proteins are localized in vestibular ganglion neurons and in their peripheral sensory extensions as early as gestational day 14. While the entire periphery of these fibers is labeled during embryogenesis, both proteins are subject to relocation during the postnatal maturation of these fibers. In the mature vestibular receptors they disappear from the fibers themselves but are found concentrated in their intraepithelial endings and in the neuronal cell body. These observations show that the distribution pattern of Synapsin I and Synaptophysin in peripheral extensions of vestibular afferent neurons during development is identical to that described in axonal processes of CNS neurons. This suggests that the peripheral processes of the vestibular afferent neurons present structural and biochemical characteristics of axons. These characteristics are consistent with a bimodal sensory and secretory function of mature endings.

Aging↗
PubMed1993

Injections of calmidazolium chloride into the ipsilateral medial vestibular nucleus or fourth ventricle reduce spontaneous ocular nystagmus following unilateral labyrinthectomy in guinea pigs.

The effects of three injections (0.5-4.5 h post-operation) of 1-[bis-(p-chlorophenyl)methyl]-3-[2,4-dichloro-beta-(2,4- dichlorobenzyloxy)phenethyl]-imidazolium chloride (calmidazolium chloride, R24571), into the ipsilateral medial vestibular nucleus or fourth ventricle, on vestibular compensation for unilateral labyrinthectomy was studied in guinea pigs. R24571, a calmodulin antagonist and inhibitor of several Ca(2+)-dependent enzymes, caused a significant reduction in the average frequency of spontaneous ocular nystagmus (spontaneous nystagmus) during the first 53 h following unilateral labyrinthectomy (n = 5), compared with vehicle-injected animals (n = 5). Although a statistical analysis was not performed on the yaw head tilt and roll head tilt data because of the large variability between animals over the 53-h period of compensation, most R24571-treated animals had less yaw head tilt (4/4 animals) and roll head tilt (4/5 animals) at 9-11 h post-labyrinthectomy than the average values for the vehicle groups at that time. The decrease in the frequency of spontaneous nystagmus following R24571 treatment was not associated with general ataxia or sedation. These results are consistent with recent biochemical studies in suggesting that intracellular pathways associated with Ca2+ may be involved in the neuronal mechanisms of vestibular compensation following unilateral labyrinthectomy.

Animals↗
PubMed1994

N-methyl-D-aspartate receptors contribute to afferent synaptic transmission in the medial vestibular nucleus of young rats.

In the medial vestibular nucleus (MVN), the non-N-methyl-D-aspartate (NMDA) subtype of ionotropic glutamate receptors has been reported as operating at synapses between ipsilateral vestibular afferents and neurons. In the present study, we addressed the question of whether or not NMDA receptors contribute to afferent synaptic transmission in the MVN and if so, to what degree. Using nystatin-perforated or conventional whole-cell patch clamp methods in brainstem slices of young rats (postnatal day 4-6), we found that NMDA receptors contribute to a substantial extent to afferent synaptic transmission in the MVN of young rats.

2-Amino-5-phosphonovalerate↗
PubMed1989

Neurotransmitter effects on inhibitory burst neurons in the cat.

The present experiment was designed to determine which neurotransmitter influences the burst pattern in the firing of the inhibitory burst neurons (IBN) during vestibular nystagmus. Cats were anesthetized with ether and mounted in a stereotaxic apparatus on a turntable, implanted stimulation electrodes, removed occipital bone and aspirated the vermal part of cerebellum. After the operation ether was discontinued. The recordings took place with the cats in an alert condition created by upper cervical cord transsection, artificial respiration and local anesthesia by infiltrating 0.5% lidocaine into the semilunar ganglions every two hours. We also employed iontophoretic application of the various drugs: GABA, muscimol, glycine, serotonin (5-HT) and bicuculline through seven-barrelled glass micropipettes. GABA or muscimol did not influence nystagmus rhythm, but both chemicals caused strong suppression of burst activities in IBN. Since this inhibitory effect of GABA was suppressed by the simultaneous application of bicuculline, IBNs appear to be controlled by GABAA receptor. Glycine and 5-HT did not change the firing pattern of IBN. Application of bicuculline itself caused an increase of tonic discharges of IBN. These findings suggest that IBN receive inhibitory impulses from the higher GABAergic neurons.

Animals↗
PubMed1982

The origin of efferent fibers to the inner ear in a turtle (Terrapene ornata). A horseradish peroxidase study.

The origin of efferent acoustic and vestibular fibers was determined in the turtle Terrapene ornata. After injection of an aqueous solution of horseradish peroxidase (HRP) into either the cochlear duct or into the ampullae of the horizontal and anterior semicircular canals, neurons in the medullary reticular formation were labeled by the reaction production of retrogradely transported HRP. These neurons were located bilaterally in the medial reticular nucleus. The majority were found ipsilateral to the injection site. There was no demonstrable difference in size, shape, and labeling pattern between efferent acoustic and efferent vestibular neurons. The crossed component component of efferent acoustic fibers, however, was rather sparsely developed.

Animals↗
PubMed2004

Gaze-related response properties of DLPN and NRTP neurons in the rhesus macaque.

The dorsolateral pontine nucleus (DLPN) and nucleus reticularis tegmenti pontis (NRTP) are basilar pontine nuclei important for control of eye movements. The aim of this study was to compare the response properties of neurons in DLPN and rostral NRTP (rNRTP) during visual, oculomotor, and vestibular testing. We tested 51 DLPN neurons that were modulated during smooth pursuit (23/51) or during motion of a large-field visual stimulus (28/51). Following vestibular testing, we found that the majority of smooth pursuit-related neurons in DLPN were best classified as gaze (13/23) or eye velocity (7/23) related. Only a small percentage (3/51) of DLPN neurons responded during vestibular ocular reflex in the dark (VORd). We tested rNRTP neurons as described above and found the majority of neurons (35/43) were modulated during smooth pursuit or during motion of a large-field stimulus only (4/43). A significant proportion of our rNRTP gaze velocity neurons (10/18) were also modulated during VORd. We found that the majority of smooth pursuit related neurons in rNRTP were best classified as gaze velocity (18/35) or gaze acceleration (11/35) sensitive. The remaining neurons were classified as eye position or eye/head related. We used multiple linear-regression modeling to determine the relative contributions of eye, head and visual inputs to the responses of DLPN and rNRTP neurons. Our results support the suggestion that both DLPN and rNRTP play significant roles not only in control of smooth pursuit but also in control of gaze.

Action Potentials↗
PubMedDate not supplied

Effect of transverse temporal bone fracture on the fluid compartment of the inner ear.

Five temporal bones exhibiting transverse fractures were studied with a view to determining whether such fractures could lead to symptomatic endolymphatic hydrops. Four out of the five temporal bones showed the fracture line traversing the vestibular aqueduct. Two of these four showed complete obstruction of the endolymphatic duct. One of these had an intact membranous labyrinth and severe endolymphatic hydrops. The other had ruptures of the membranous labyrinth and no hydrops. Three ears exhibited partial preservation of auditory and vestibular hair cells and neurons. These findings are consistent with the concept that a transverse fracture may produce endolymphatic hydrops by obstructing the vestibular aqueduct while preserving enough audiovestibular epithelium and neurons to present as symptomatic Menière's disease.

Adult↗
PubMed1989

Vestibulospinal findings in two syndromes with spontaneous vertigo attacks.

The influence of vestibular dysfunction upon the vestibulospinal reflex (VSR) in two common peripheral syndromes was investigated by two types of posturographic examination: "static" posturography, recording and analyzing the postural sway in stance, and "kinetic" posturography, recording the stepping in place test. The influence of the dysfunction was examined outside the attacks, ie, between attacks and not during or immediately after an attack, in patients with Meniere's disease and in others with a sudden vestibular loss syndrome, "neuronitis." However, in both syndromes the influence of the dysfunction was obvious only in some patients; this indicates that central adaptation intervened in the other patients. In this way, central compensation related to the VSR was assessed and compared with compensation for the vestibulo-ocular reflex assessed by the rotation tests. Discordance was shown in a number of cases, ie, a number of cases showed compensation for one reflex, but not for the other. Comparison of the results of both posturographic methods also showed discordance. Normal performance in the walking test could not always be correlated with normal performance in the standing test and vice versa.

Humans↗
PubMed1998

Autonomic reaction to vestibular damage.

The vestibular system provides inputs to many neurons in the brain stem that participate in autonomic control. This multiplicity of vestibular-autonomic connections plays a variety of roles. Whereas it has been known for decades that unilateral vestibular lesions can result in motion sickness, recent data suggest that the vestibular system participates in making adjustments in blood pressure and respiration that are necessary to maintain homeostasis during movement and changes in posture. Animals with bilateral vestibular lesions are more susceptible to posturally related hypotension than vestibularly intact animals, and it is also possible that orthostatic hypotension after space flight is caused in part by microgravity-related changes in otolith function. Patients with vestibular lesions could also be more vulnerable to respiratory disturbances related to posture, such as obstructive apnea. Vestibular dysfunction has additionally been linked with anxiety disorders, such as agoraphobia, which may result from alteration of vestibular inputs to brain stem monoaminergic neurons (which are known to process these signals). Even sleep disturbances might be connected with vestibular disorders because neurons in the pontine reticular formation that are critical in switching between sleep states may be influenced by labyrinthine inputs. Thus it is likely that vestibular damage will result in a number of parallel disturbances in autonomic function.

Animals↗