[Antidromic and synaptic activation of frog vestibular neurons by stimulation of the vestibular nerve].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The morphology of secondary vertical vestibular neurons was investigated by injection of horseradish peroxidase (HRP) into cells connected to the posterior canal system in rabbits (lateral-eyed animals) and cats (frontal-eyed animals). Vestibular neurons were identified by stimulation with bipolar electrodes implanted into the ampullae of the anterior and posterior (PC) semicircular canals of pigmented rabbits; in the cat, these cells were identified by natural and electrical stimulation. Axons monosynaptically activated by PC stimulation were injected with HRP in the medial longitudinal fasciculus (MLF). These were later reconstructed by light microscopy after the brains had been processed with a DAB-CoCl2 method. In the rabbit the majority of the axons bifurcated after crossing the midline with one branch ascending and the other descending in the MLF. The ascending branches gave rise to collaterals that terminated in both the trochlear nucleus and the inferior rectus subdivision of the oculomotor nucleus. In addition some axons also sent collaterals into the paramedian pontine reticular formation, the periaqueductal grey and the interstitial nucleus of Cajal. The descending branches were followed to the caudal part of the medulla in the MLF and gave rise to collaterals terminating in the vestibular nuclei, the medullary reticular formation, the perihypoglossal nuclei, the abducens nucleus, and the facial nucleus. In another cell type axons crossed the midline without giving off any collaterals and proceeded caudally in the caudal MLF. The synaptic effects of the two types of cells were concluded to be excitatory and inhibitory, respectively. Cell bodies of contralaterally projecting neurons were located in either the medial or ventro-lateral vestibular nuclei. In the cat we observed two neuron classes, with contralaterally projecting axons, whose synaptic effects are presumably excitatory. Their cell somata were located in the medial vestibular nucleus. Termination patterns were similar to both the trochlear and oculomotor nuclei, but neither projected to the abducens nucleus. One class of neurons was almost identical to that found in the rabbit with the main axon bifurcating in the MLF. The second type lacked a descending branch in the MLF. Axon collaterals of the latter type crossed the midline within the oculomotor nucleus after terminating in the inferior rectus subdivision to reach a similar portion of the ipsilateral oculomotor nucleus. Collaterals of these axons also terminated bilaterally in the supraoculomotor region between trochlear and oculomotor nucleus, the interstitial nucleus of Cajal and prerubral loci (including the fields of Forel). In similarity to the rabbit, presumed inhibitory vestibular neurons were found with axons directed caudally in the MLF without brain stem collaterals.(ABSTRACT TRUNCATED AT 400 WORDS)
The aim of this work was to verify whether and how spontaneous or glutamate(GLU)-induced enhancements of the neuronal firing rate modified the responsiveness of the vestibular neurons to microiontophoretic application of serotonin (5-HT). During experiments performed on anaesthetized Wistar rats the responses to 5-HT applications were studied in neurons of the lateral vestibular nucleus identified by the antidromic activation upon stimulation of the vestibulospinal tract. The magnitude (in percent) of the 5-HT induced excitatory responses decreased (hyperbolic correlation, r = 0.91) when the background mean firing rate was enhanced spontaneously or by long-lasting application of GLU. Even in high-discharging units, the response never changed its sign. The trend to a depression of the response to 5-HT in function of the background discharge was observed when either the enhancement of firing occurred spontaneously and it was induced by an application of GLU, no significant difference (F-test) being found between the two cases. It is concluded that serotoninergic afferents can exert a strong control upon the vestibular neurons when the background activity is depressed, and only a weak influence when the neuronal firing is enhanced by other excitatory afferents. It remains to verify whether the type of interference observed between GLU and 5-HT is specific or can be also detected between 5-HT and other excitatory neuromediators.
A serovirological study to clarify the pathogenesis of vestibular neuronitis was made on 44 patients. The diagnosis of vestibular neuronitis was made under the diagnostic criteria. Sera from all 44 cases were collected twice or more at defined intervals. Of these, 36 cases were treated as paired sera. Seventeen out of 36 paired cases showed significant change in serum viral antibody titer (HSV, 2 cases; CMV, 1 case; EBV, 7 cases; rubella, 2 cases; adeno., 2 cases; influ. A, 1 case; influ. B, 2 cases). It was assumed that infection caused by these detected viruses played an important role in the onset of vertigo in each case.
Scarpa's ganglion and the superior vestibular nerve of a patient with vestibular neuronitis examined under the electron microscope displayed degenerative neuronal changes and axonal lesions considered to be the cause of the clinical features of vestibular neuronitis.
BACKGROUND: Lyme disease has been described as one possible cause of sudden sensorineural hearing loss and vestibular neuronitis. The necessity of serological diagnosis and its therapeutic consequences have been discussed controversially. PATIENTS AND METHODS: 344 patients with acute sensorineural hearing loss and 66 patients with vestibular neuronitis were examined in retrospect. By means of ELISA (Enzygnost Borreliosis, Dade Behring Marburg) the specific prevalences of IgG- and IgM-antibodies against borrelia in serum were evaluated. The frequency of seroprevalences for both diseases were compared to those given in the literature. Neurootological findings of the seropositive patients were compared with those of seronegative and analysed statistically. RESULTS: 15.7 % of the patients with sudden sensorineural hearing loss had positive levels of IgG-antibodies. IgM-titers were elevated in 4.7 % of the patients. The seroprevalences for IgM and IgG were above those described by other investigators for the healthy population. Patients with positive IgM-antibodies showed more often low frequency hearing loss than IgG-positive patients. 18.2 % of the patients with neuronitis vestibularis had IgG- and 1.5 % IgM-antibodies against Borrelia. Whereas IgG occurred more often than known for the healthy population, IgM was within the limit for the healthy population. The seropositive group did not show any remarkable neurootological signs compared with the seronegative group. CONCLUSIONS: Because of the elevated seroprevalences Borrelia infections may be one possible but very rare cause of sudden sensorineural hearing loss and vestibular neuronitis. Low frequency hearing loss may be a sign for an infection with Borrelia as an etiological factor especially in combination with seropositive titers. In case of the presence of IgM-antibodies, patients may be treated with oral antibiotics (Doxycyclin, Cefuroxim). In patients with neuronitis vestibularis a neuroborreliosis should be excluded by means of lumbar puncture.
Recent advances in magnetic resonance imaging (MRI) have demonstrated facial nerve enhancement in facial nerve palsy and cochlea enhancement in sudden deafness. However, no report has described the findings of enhanced MRI in vestibular neuronitis. Eight cases of vestibular neuronitis were studied with enhanced MRI. We did not detect any enhanced lesions of the vestibular nerve or ganglion. So far, as the present conditions of MRI are concerned, it is difficult to detect any enhancement in the vestibular nerve and ganglion. Further study will be required to evaluate the suitability of MRI for vestibular neuronitis.
Efferent neurons innervating the vestibular labyrinth and cochlea of the pigeon have been identified by means of a variety of retrograde tracers: [3H]-adenosine (Ad), horseradish peroxidase (HRP), Evan's Blue (EB) and Bisbenzimide (Bb). Discrete injections into individual cristae ampullares of the semicircular canals, into the macula utriculi, or into several of these end organs resulted in similar patterns of neuronal labelling. Efferent vestibular neurons were always found within a small portion of the nucleus reticularis pontis caudalis (RP), ventrolateral to the abducens nucleus on both sides. No systemic difference in the locations of labelled cells was found following injection into different sensory epithelia. Cell counts following injections into individual cristae did not differ significantly from those following injections into all three cristae. The injections into all cristae in both labyrinths yielded cell counts that were much lower than twice the number of cells labelled by injections into the three cristae on one side only. When HRP was injected into the right lateral canal crista and Ad into the right posterior canal crista, a high proportion of neurons was labelled with both compounds (61% of the HRP-labelled cells and 67% of the Ad-labelled cells). Injections of EB into all three cristae on the right side and Bb into all three cristae on the left side produced a smaller percentage of doubly labelled cells (10% of the EB-labelled cells and 6% of the Bb-labelled cells). It is concluded, therefore, that there is a considerable degree of collateralization within one labyrinth. Fewer collaterals of efferent neurons are directed to both labyrinths. Since each semicircular canal represents head rotation in one direction and one plane, it is unlikely that efferents which contact several different movement sensors can provide sensory motor control that is specific for directions and planes of head movements. Control injections of these tracers into the cochlea yielded labelled cells in a different reticular structure, the nucleus reticularis paragigantocellularis lateralis (Pgc), on both sides, as well as in the RP. It is proposed that the Pgc cells represent cochlear efferents, while the RP neurons are related to the macula lagenae, an otolithic organ of balance in the pigeon.
The distribution of choline acetyltransferase messenger RNA (mRNA) among efferent vestibular neurons in the chinchilla was investigated. mRNA coding for choline acetyltransferase, the enzyme that synthesizes acetylcholine, was used as a marker for the cholinergic system. In order to retrogradely label the efferent vestibular neurons, Fluoro-gold was injected through the oval window into the inner ear of anesthetized young male chinchillas (6 to 12 months old). The animals were anesthetized and perfused through the heart 2 days post injection with 4% paraformaldehyde in phosphate buffer. Retrogradely labeled efferent vestibular neurons were mapped in brainstem sections prior to processing for in situ hybridization histochemistry using radiolabeled ribonucleic acid probes complementary to the 3' end of the choline acetyltransferase mRNA. At the levels of the ascending facial nerve and the genu of the facial nerve, we found that approximately 90% of the Fluoro-gold labeled cells in group E1 contained choline acetyltransferase mRNA. All of the group E2 cells that were labeled with Fluoro-gold were found to be cholinergic (contain choline acetyltransferase mRNA). Finally, 60% of the Fluoro-gold-labeled cells in the caudal pontine reticular nucleus contained choline acetyltransferase mRNA.
We performed steroid therapy on 34 cases with vestibular neuronitis and compared them with 77 patients not subjected to this therapy to examine the role of recovery of their vestibular function. Since no relation was noted between use of steroid and changes in subjective symptom of dizziness, the use of steroid is likely to facilitate the disappearance of spontaneous nystagmus in the early recovery stage. Canal paralysis recovered significantly by steroid and in cases of slight and moderate paralysis at the onset, recovery was more significant. Steroid therapy is argued to be effective for the recovery of vestibular function in cases of vestibular neuronitis.
The aim of the present research was to evaluate the effects induced by arginine vasopressin (VP) microinjection on the electrical activity of single vestibular neurons. Experiments were performed on anaesthetized guinea-pigs in which the spontaneous and the evoked electrical activity of vestibular neurons were recorded before and after intranuclear VP microinjection (0.25.10(-5) pg VP in 0.25 microliter NaCl 0.9% solution). Results showed that VP microinjection affects the spontaneous as well as the evoked vestibular neuron activity. More precisely, 60% of 30 tested neurons were inhibited, 30% were excited and the remaining 10% were unaffected by VP microinjection. The changes in neuronal activity reported above were attributed to a direct action exerted by the polypeptide on vestibular complex neurons. The possible role played by VP in the mechanisms of postural control exerted by the vestibular system was considered as well.
Untangling the molecular and physiological interactions that generate the proper connections of the primary vestibular neurons in normal gravity requires two parallel approaches. One approach needs to use mutant mice to delineate the molecular basis of developmental mechanisms that govern ear development, including formation and differentiation of neurons and establishment of their peripheral and central connections. Beyond that and in addition to it, we need physiological investigations using microgravity and/or hypergravity, as well as absence of otoconia, to understand the role played by vestibular stimuli to fine tune connections of primary and secondary vestibular neurons. This paper provides an overview of some of the molecular mechanisms uncovered over the last few years that guide development, differentiation and survival of primary vestibular neurons of the mammalian ear. Briefly, several genes that are essential for primary neuron formation have been identified, all genes that govern embryonic survival are known and the first genes and mechanisms that guide formation of proper connections are being revealed. While still incomplete, the progress has been astounding and the completion of the mouse genome project will further accelerate the pace. Such data pave the way to put the research on the influence of altered gravity stimulation within a molecular framework.
An epidemiological survey of vestibular neuronitis in Japan was done using a questionnaire. Answer sheets were obtained from 619 patients with vestibular neuronitis. In order to evaluate data from aged patients, 74 cases were singled out. The following results were obtained: i) There was no sexual difference and no laterality of affected side; ii) There was no case of bilateral vestibular neuronitis; iii) Ten cases were reported as recurrent. Aged patients had a relatively high rate of recurrence; iv) About 10% of 74 cases had had an upper respiratory tract infection, and this rate was lower than that for patients under 65 years of age; v) Thirty-five cases had complications. Hypertension was the most common complication; vi) The caloric test was re-used in 28 cases. The continued existence of caloric CP was observed in 23 cases upon re-examination.
Over a 14-year period commencing in 1973, we followed 177 children less than 12 years old suffering from vertigo and/or disequilibrium. In 35 of 177 patients, the vertigo-like condition was due to peripheral causes: 10 sudden deafness, six vestibular neuronitis, three benign paroxysmal positional vertigo and three Meniere's disease. In this paper, two cases of pediatric vestibular neuronitis will be reported in detail. All six patients with vestibular neuronitis were boys, and the affected sides were equally distributed in the group. The patients recovered within two to four weeks, a prognosis which is better than that observed in adults. With regard to directional nystagmus, the gaze was bilateral in five patients and vertical in two. They showed neuro-otologic findings that suggest not only unilateral dysfunction but also bilateral disorders or partial lesions on the central vestibular system. Consequently, in the hope that the study of vertigo in childhood may provide additional clues to the pathogenesis of the disease in adults, we would like to consider two cases of pediatric cases of vestibular neuronitis.
The aim of this work was an analysis of caloric directional preponderance prevalence in patients with vestibular neuronitis and coincidence of above mentioned symptoms with spontaneous and positional nystagmus. The examinations were carried out in 36 patients, aged 27-51, 19 women and 17 men. The vestibular reactions were recorded by electronystagmography and directional preponderance and mean angle velocity of the slow phase were calculated. It was pointed out that in vestibular neuronitis patients the directional preponderance may appear early and in great number of cases with canal paresis. However, in the late stages of vestibular neuronitis the directional preponderance may appear independently without the spontaneous and positional nystagmus.
We evaluated vestibular function, especially for positional, head shaking and caloric nystagmus, in 43 patients with vestibular neuronitis, for long periods from the onset. The results suggested that in these cases of vestibular neuronitis, which were studied for more than 10 years after onset of the disease, the disease may still be in the uncompensated stage or may have worsened in the partially compensated stage.
Eighty-one cases with vestibular neuronitis were examined. The diagnostic criteria were a sudden onset of vertigo without previous symptoms, spontaneous nystagmus towards the healthy side, totally extinguished caloric responses with 44 degrees C and 30 degrees C water irrigation and no involvement of hearing associated with the onset of the disease. The series was divided into a prospective and a retrospective group. The prospective group A was examined at the acute stage, about 1 month and 1 year afterwards. The retrospective group B fulfilled the same criteria as group A and was examined 1-8 years after the acute stage. The results of the acute stage in group B were analysed from the case history reports, electronystagmo- and audiograms. The preceding and predisposing factors and symptoms were inquired. The examination scheme included the clinical otoneurological examination, the nystagmographic, audiological and clinical neurophysiological measurements and the serological and hematological specimens were collected at the acute stage of group A to examine the role of virus infections in the etiology of vestibular neuronitis. The liquor specimens of 16 cases available in group A were analysed. A recent respiratory infection was reported by 9 cases (27.3 percent) in group A and by 18 cases (37.5 percent) in group B. The serological evidence (increase of IgM-antibodies) was observed in 1 case against influenza A and in 1 case against parainfluenza 3 and the hematological examinations revealed clues of virus infection in 6 cases (18.2 percent) of group A. Cell counts and protein analyses of the liquor specimens were within normal limits. Cases with arterial hypertension under medical control were observed in 15.2 percent of group A and 14.6 percent in group B. These figures do not exceed the age- and sex-correlated prevalence of arterial hypertension in Finnish population. The clinical symptoms included an acute chiefly rotatory vertigo associated with nausea and vomiting without subjective involvement of hearing. The prominent symptoms lessened gradually during the first week and most of the patients were able to their earlier work after one month. The prognosis of the disease was good. The clinical otoneurological findings of the acute stage included spontaneous nystagmus with Frenzel's glasses and disturbances of the vestibulospinal tests. These abnormalities improved markedly during the follow-up period. The results of electronystagmography were characteristic of a pure peripheral vestibular disorder. Nystagmic beats were observed almost regularly in the pendular eye-tracking test at the acute stage examination.(ABSTRACT TRUNCATED AT 400 WORDS)
The activity of medial vestibular nucleus neurons projecting to the contralateral abducens nucleus (premotor vestibular neurons) has been recorded during spontaneous and vestibular induced eye movements in the alert cat. Recorded neurons were identified by their antidromic activation from the abducens nucleus and by the post-synaptic field potential induced in this nucleus. The activity of identified medial vestibular neurons increased significantly with horizontal eye position and velocity toward the contralateral side, and decreased abruptly during ipsilateral saccades. The activity of these neurons was also related to head velocity toward the ipsilateral side. The functional role and origin of eye position and velocity signals present in these vestibular neurons are discussed.