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PubMed1995

Post-natal development of tonic activity and membrane excitability in mouse medial vestibular nucleus neurones.

The development of tonic activity and membrane excitability of MVN neurones was examined using extracellular and intracellular recordings in slices prepared from mice at various stages in the first post-natal month. The tonic spontaneous discharge rates of MVN cells as post-natal day 5 (P5) were typically below 5 imp/s, and gradually increased to reach adult values of 11-20 imp/s by P30. While most MVN cells at P5 were electrophysiologically immature, by P10-P15 they had developed overshooting sodium spikes and pacemaker conductances which generated a steady discharge of spontaneous action potentials. From the earliest stages when tonic activity was observed, immature forms of the adult Type A and Type B action potential shapes could be recognized in tonically active cells. There was a marked rostro-caudal gradient in the time course of the maturation of MVN neurones, with cells in the rostral part of the MVN firing at higher rates and having more mature action potential shapes than caudally located cells.

Action Potentials↗
PubMed2003

Activity-related postlesional vestibular reorganization.

The synaptic convergence patterns of semicircular canal and macular afferent nerve inputs onto second-order vestibular neurons reorganize in adult frogs after a change in the activity of vestibular nerve afferent fibers. Axotomized afferent nerve fibers become silent after a vestibular nerve lesion, and second-order vestibular target neurons become disfacilitated. These changes initiate an activity-related process that was studied in detail in vitro two months after a section of the ramus anterior (RA) of N. VIII. The postlesional reaction results in an expansion of signals, preferentially from intact, remaining afferent nerve fibers, but also from excitatory commissural and spinal ascending fibers. This process of expansion takes weeks, is graded in its extent, and reversible in case of a nerve regeneration, but is not competitive, i.e., the synaptic contacts from axotomized afferent nerve fibers are maintained without a change in their efficacy. Postlesional synaptic reorganization in the brainstem is restricted to the operated side, underlies the improved responsiveness of disfacilitated second-order vestibular neurons, but also their altered spatial response tuning. The functional consequences of this reorganization were studied in vivo two months after RA nerve section by recording abducens nerve responses during linear or angular accelerations. The vector orientations of best responses of the abducens nerve of chronic RA frogs evoked by linear or angular acceleration differed from the vector orientations of controls. In chronic RA frogs, linear acceleration evoked contralesional abducens nerve responses that originated from the utricle on the intact side and from the lagena, a vertical macular organ in frogs. Such an inadequate lagenar response component was absent in controls and in the ipsi-lesional abducens nerve of chronic RA frogs. Similar differences were detected in the direction of abducens nerve responses of chronic RA frogs during angular acceleration. Thus, compensatory vestibulo-ocular reflexes of chronic RA frogs became more symmetric in gain, but less precise in direction.

Abducens Nerve↗
PubMed1980

Responses of vestibular nucleus neurons in the visually deprived cat to optokinetic stimulation of central parts of the visual field.

Single cells were recorded in the vestibular nucleus of normal and monocularly deprived cats and stimulated by slowly drifting large area visual patterns. We found no difference in response strength, direction specificity and binocular influence between the neurons recorded in normal and in monocularly deprived cats. This makes it very unlikely that the nucleus of the optic tract (NOT) in the pretectum provides a strong direct input to the vestibular nuclei to modulate their activity with visual stimulation.

Animals↗
PubMed1995

[The influence of rates of pressure change on pressure-induced vestibular response in guinea pigs].

Ambient pressure changes are known to induce vertigo and bodily disequilibrium, e.g. alternobaric vertigo. It is predicted, based on clinical observations of such vertigo, that the rates of pressure change are responsible for alternobaric vertigo. The aim of the present study was to clarify the influence of the rates of pressure change on the activities of primary vestibular neurons using an animal model of alternobaric vertigo. The responses of primary vestibular neurons to middle ear pressure stimuli were investigated in guinea pigs under 2 different rates of pressure change (+/- 50, +/- 100 mmH2O/sec). The following results were obtained. 1. The response rates and the gains of firing rates with pressure stimuli were larger under +/- 100 mmH2O/sec than under +/- 50 mmH2O/sec. 2. The onsets of responses to pressure stimuli were faster under +/- 100 mmH2O/sec than under +/- 50 mmH2O/sec. The results obtained in the present study reveal that vestibular activities are altered by the rates of ambient pressure change.

Animals↗
PubMed2002

Symptoms of vertigo in general practice: a prospective study of diagnosis.

BACKGROUND: There is little published evidence of the general practice experience of the diagnostic outcomes when symptoms of vertigo present. What research there is has been dominated by specialist centres. This gives a skewed view of the prevalence of the causes of such symptoms. AIM: To describe the likely diagnosis of symptoms of vertigo. DESIGN OF STUDY: Prospective cohort study METHODS: Thirteen GPs were recruited and trained to clinically assess and follow up all patients presenting with symptoms of vertigo over a six-month period Age-sex data were simultaneously gathered on those who consulted with non-vertiginous dizziness. RESULTS: The main diagnoses assigned by the GPs in 70 patients were benign positional vertigo, acute vestibular neuronitis and Ménière's disease, which together accounted for 93% (95% confidence interval = 71% to 100%) of patients' symptoms. Ninety-one per cent of patients were managed in general practice and 60% received a prescription for a vestibular sedative. CONCLUSION: This study suggests that presentations of symptoms of vertigo can be clinically diagnosed in most cases. The diagnoses recorded by GPs differ in proportion to those in specialist centres, with a larger number of patients suffering from benign positional vertigo and acute vestibular neuronitis in general practice, in contrast with specialist centres, which see more patients with Ménière's disease.

Diagnosis, Differential↗
PubMed2000

Regional and cellular distribution of protein kinase C in rat cerebellar Purkinje cells.

Protein kinase C (PCK) is a family of isoforms that are implicated in subcellular signal transduction. The authors investigated the distribution of several PKC isoforms (PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon) within major cerebellar cell types as well as cerebellar projection target neurons, including Purkinje neurons, cerebellar nuclear neurons, and secondary vestibular neurons. PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon are found within the cerebellum. Of these isoforms, PKC-gamma and PKC-delta are highly expressed in Purkinje cells. PKC-gamma is expressed in all Purkinje cells, whereas the expression of PKC-delta is restricted to sagittal bands of Purkinje cells in the posterior cerebellar cortex. In the lower folia of the uvula and nodulus, Purkinje cell expression of PKC-delta is uniformly high, and the sagittal banding for PKC-delta expression is absent. Within the cerebellar nuclei, PKC-delta-immunolabeled axons terminate within the medial aspect of the caudal half of the ipsilateral interpositus nucleus. PKC delta-immunolabeled axons also terminated within the caudal medial and descending vestibular nuclei (MVN and DVN, respectively), the parasolitary nucleus (Psol), and the nucleus prepositus hypoglossi (NPH). PKC-gamma-immunolabeled axons terminated in all of the cerebellar nuclei as well as in the lateral and superior vestibular nuclei and the MVN, DVN, Psol, and NPH. The projection patterns of PKC-immunolabeled Purkinje cells were confirmed by lesion-depletion studies in which unilateral uvula-nodular lesions caused depletion of PKC-immunolabeled terminals ipsilateral to the lesion in the vestibular complex. These data identify circuitry that is unique to cerebellar-vestibular interactions.

Animals↗
PubMed1976

[The activity of motor units of the musculus splenius capitis in pheripheral vestibular lesions (author's transl)].

The activity of single motor units of the splenius-capitis muscle of healthy human subjects and patients with unilateral vestibular lesions was recorded by means of microelectrodes. The major part of these units reacted to vestibular stimulation in the same way as primary and secondary vestibular neurones of other vertebrates. The reactions of these units to trapezoidale stimuli is identical to that of vestibular neurones. An angular acceleration of more than 0.6 degrees/s2 is for these units a stimulus which is above threshold, this too corresponds to findings in the vestibular nerve. In patients with unilateral vestibular lesions the threshold for rotatory stimuli is markedly increased on the side of the lesion, whereas the threshold on the other side remains constant. This method is very sensitive and vestibular lesions can be detected which cannot be seen using the common technics for vestibular examination.

Action Potentials↗
PubMed2001

Betahistine produces post-synaptic inhibition of the excitability of the primary afferent neurons in the vestibular endorgans.

Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work was to study the action of betahistine in the vestibular endorgans. Experiments were done in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 microM to 10 mM; n = 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 microM. To define the site of action of betahistine, its interactions with the nitric oxide synthase inhibitor NG-nitro-L-arginine (3 microM) and with the cholinergic antagonists atropine (10 microM; n = 3) and d-tubocurarine (10 microM; n = 3) were studied. The action of betahistine when co-administered with these drugs was the same as that in control experiments, indicating that its effects did not include nitric oxide production or the activation of cholinergic receptors. In contrast, 0.01-1 mM betahistine reduced the excitatory action of kainic acid (10 microM; n = 6) and quiscualic acid (1 microM; n = 13). These results indicate that the action of betahistine on the spike discharge of afferent neurons seems to be due to a post-synaptic inhibitory action on the primary afferent neuron response to the hair cell neurotransmitter.

Ambystoma↗
PubMed1994

The first developing "mixed" synapses between vestibular sensory neurons mediate glutamate chemical transmission.

In the present study, the nature of the synaptic transmission responsible for a monophasic potential generated by vestibular nerve stimulation of the principal cells in the chick tangential nucleus was established. This work was performed in slice preparations at the critical embryonic age of 15-16 days, the time of first observation of morphologically mixed (chemical and electrical) synapses at the axosomatic endings called spoon endings. The spoon endings are formed by the primary vestibular fibers with the largest diameters, the colossal vestibular fibers. This monophasic potential fits the criteria for chemical rather than electrical transmission due to the following responses in most cases: (i) the absence of collision between a direct spike initiated by depolarization in the principal cell and a vestibular-evoked action potential; (ii) failure to follow high frequency stimulation (up to 50 Hz); (iii) sensitivity to low calcium solution (0.1 mM). These tests indicate that strong electrical coupling between spoon endings and principal cells does not prevail at this stage. The recordings were obtained from principal cells injected intracellularly with biocytin, allowing their identification by morphological criteria. The lack of tracer coupling between the stained principal cells and their innervating vestibular fibers (n = 17) is consistent with the absence of electrical coupling. Identification of the neurotransmitter involved in this vestibular response was achieved by bath application of glutamate receptor antagonists, DL-2-amino-5-phosphonovaleric acid (40 microM) and 6-cyano-7-nitro-quinoxaline-2,3-dione (10 microM), which blocked transmission reversibly. These results suggest that at the onset of formation of these "mixed" vestibular synapses, the gap junctions identified morphologically are likely not functional, and that the main response of the principal cells to vestibular nerve stimulation is mediated by glutamate.

2-Amino-5-phosphonovalerate↗