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PubMed1987

Recording of short-latency vestibular evoked potentials induced by acceleration impulses in experimental animals: current status of the method and its applications.

The short-latency vestibular evoked potential (VsEP) induced by angular acceleration impulses (maximal amplitude 30,000 deg/sec2, rise time 2-3 msec) was recorded by skin electrodes in intact cats after various surgical and pharmacological procedures. The normal VsEP consists of 5-8 waves, several microvolts in amplitude, during the first 10 msec. The latency of the first wave (P1) is about 2 msec with respect to the start of head acceleration. The first and the second waves (P1 and P2) were shown to originate from the vestibular nerve and nucleus, respectively. The VsEP disappears permanently after bilateral labyrinthectomy, excision of the 8th nerves, or administration of large doses of gentamicin. Temporary disappearance is caused by anoxia induced for a brief period of time or injection of lidocaine (4%) into the vestibular nerve or into the inner ear after contralateral labyrinthectomy. The VsEPs in the intact cat are similar whether clockwise or counterclockwise stimuli are used and are not affected by changing the position of the head. Unilaterally labyrinthectomized animals, however, show asymmetric response whereby excitatory stimulation of any of the intact semicircular canals evokes prominent P1 and P2 waves which are absent with inhibitory stimulation. The rate and input-output intensity functions of the VsEP are described. The threshold of the VsEP was found to be 1000-1500 deg/sec2. In addition to the neurogenic waves, 2 other potentials appear occasionally in the response: large-amplitude and longer-duration waves with latencies of 8-20 msec, which are of myogenic origin, and smaller waves with shorter latency which probably represent vestibular microphonics and generator potentials. Extracellular recordings of the responses of single second-order neurons in the vestibular nuclei to the same acceleration impulses confirmed that the kinetic vestibular neurons can respond to these stimuli with a latency as short as 3.5 msec. This method for inducing and recording VsEPs has proved to be a powerful tool for the evaluation of vestibular function in experimental animal models.

Acceleration↗
PubMed1993

Medial vestibular nucleus in the guinea-pig: histaminergic receptors. II. An in vivo study.

In a companion paper (Serafin et al. 1992) we have demonstrated in vitro that histamine depolarizes three previously described medial vestibular nucleus neuron (MVNn) types (Serafin et al. 1991a, b). It has also been shown that this effect was exclusively mediated through postsynaptic H2 receptors. All the same, the eventual contribution of presynaptic H3 receptors to the physiological response of the MVNn to histamine remained an open question since, during the slicing procedure, any histaminergic axons projecting to the vestibular nuclei would have been interrupted. This rendered our study of H3-mediated effects of histamine difficult. Hence, in the present in vivo study our aim was three-fold: (1) to investigate the presence of H3 receptors at the vestibular nuclei level; (2) to evaluate the functional importance of MVNn H2 receptors; and (3) to explore whether H3 ligands, when injected intraperitoneally (i.p.), could modulate dynamic vestibular functions. In order to address the first two questions, we investigated postural changes induced by perfusion of the guinea-pig's vestibular nuclear complex with specific ligands of the H2 and H3 receptors. Our data extend the conclusions of our in vitro study and suggest that lateral vestibular nuclei neurons and the MVNn are endowed with both H2 and H3 receptors. Our results indicate furthermore that histamine can modulate, quite effectively, static vestibular reflexes. Finally, the present study demonstrates that i.p. injection of thioperamide, an H3 antagonist, induces a significant decrease in the horizontal vestibular-ocular reflex gain and, by contrast to most of the clinically used antihistaminics, has no detrimental effect on the alertness level. Our results may thus lead to clinical testing and use of H3 antagonists as antivertigo or anti motion-sickness drugs.

Animals↗
PubMed2005

Effects of betahistine on the spatiotemporal response properties of vestibulospinal neurons to labyrinthine volleys.

Betahistine, a drug used in the treatment of vestibular disorders, speeds-up the recovery from hemilabyrinthectomy in experimental animals, likely through the activation of histamine receptors. In order to better understand the mechanism of action of this drug we investigated, in adult, urethane anesthetized rats, whether betahistine modifies the spatial (directional) and temporal response properties of vestibular nuclear neurons to the labyrinthine input, as well as the convergence of different labyrinthine signals on single units. Extracellular single-unit activity was recorded from the caudal, spinal-projecting region of the vestibular nuclei during tilt of the animal, before and after i.p. injection of betahistine. The two orthogonal directions of maximal and minimal response to tilt, as well as the corresponding gains were determined for each neuron. Betahistine reduced the maximal response gain of units showing larger basal values of this parameter and increased it in neurons with smaller basal values, while the minimal response gain was on the average raised. These changes led to a significant decrease in the spatial specificity of the neurons, suggesting that betahistine affects the process of spatiotemporal convergence on vestibular units, likely through a rearrangement of the various inputs. This could be related to the effect of the drug on vestibular compensation.

Acoustic Stimulation↗
PubMed2003

Properties of neurons from the rat medial vestibular nucleus in microexplant culture.

This study is a first step in an attempt to identify the factors which determine and maintain the electrophysiological phenotype(s) of mature neurons of the medial vestibular nucleus (MVN). We cultured MVN microexplants obtained from slices of the brainstem of newborn rats, using a hollow punching needle. The electrophysiological maturation of the neurons was followed by analyzing their responses to 1 s steps of current of increasing amplitude. The maximal number of spikes that was generated in response to such stimuli increased dramatically over time in vitro. However, even after 28 days in vitro, it did not exceed about 60 spikes/s. At this stage of culture, the input-output properties of the spike generator of the MVN neurons were similar to those observed in brainstem slices of newborn rats, but clearly inferior to those of adult neurons which can generate sustained firing up to 150-200 spikes/s.

Action Potentials↗
PubMed1995

Properties of superior vestibular nucleus flocculus target neurons in the squirrel monkey. II. Signal components revealed by reversible flocculus inactivation.

1. Seven upward eye velocity flocculus target neurons (FTNs) and two flocculus projecting neurons (FPNs) were studied before and after ipsilateral flocculus inactivation by injection of muscimol in the alert squirrel monkey. An additional seven FTNs and seven FPNs recorded from the corresponding FTN and FPN areas were recorded after injection. Response properties of FTNs and FPNs were characterized by visual-vestibular interaction paradigms and were compared before and after flocculus inactivation. 2. In FTNs the mean firing rate increased within 2-5 min after muscimol injection in the flocculus and reached a plateau level in approximately 10-20 min. The average mean firing rate for seven FTNs increased from 117 to 174 spikes/s, a net increase of 57 spikes/s (49%). Accompanying the large increase of the mean firing rate, a spontaneous nystagmus in the darkness developed with the slow phase directed upward and contralateral. 3. The firing rate modulation during visual following of a sinusoidal optokinetic drum (0.5 Hz) decreased within 2-5 min after muscimol injection in the flocculus and reached a level of 0 in approximately 10-20 min for all FTNs. After that, some cells remained unmodulated for the period of recording; other cells gradually reversed their phase and developed a modulation out of phase with drum velocity. The depletion of the visual following eye velocity signal on superior vestibular nucleus (SVN) FTNs accompanied a small but consistent decrease of visual following eye velocity amplitude. The average maximum decrease of eye velocity was 26 +/- 9% (mean +/- SD). 4. After flocculus inactivation, even though the modulation response at 0.5 Hz during visual following was abolished, a slow-component eye velocity signal with the same on direction was revealed by a constant-velocity optokinetic stimulus. It is concluded that there are at least two kinds of eye velocity signals during the optokinetic response. These signals are combined at the FTNs and are subsequently relayed to the oculomotor neurons. The source of the fast component is the flocculus, and the source of the slow component is another, as yet unidentified brain structure. 5. The effect of flocculus inactivation on the modulation amplitude during the vestibuloocular reflex (VOR) in darkness was variable: two cells did not change, two cells decreased, and three cells increased their amplitude. The response phase tended to move toward a phase lead, but the change was small. The effect on VOR suppression was more prominent.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Discharge properties of brain stem neurons projecting to the flocculus in the alert cat. II. Prepositus hypoglossal nucleus.

1. The aim of this study was to characterize the signals transmitted by the neurons of the nucleus prepositus hypoglossal (NPH) to the middle zone of the flocculus of the cat. The methods, the behavioral testing, and the animals used in this study were the same as those used in the accompanying paper on medial vestibular nucleus neurons. 2. The rostral two-thirds of the NPH was explored in alert animals with microelectrodes during stimulation of the middle zone of both flocculi. Discharges of neurons were analyzed during spontaneous eye movements (head fixed) and during horizontal vestibuloocular reflex (VOR) activity elicited by sinusoidal stimulation (10, 20, 30, or 40 degrees at 0.1 Hz). Forty neurons were found to be antidromically activated from only one or the other of the two flocculi (latency: 0.99 +/- 0.17 ms, mean +/- SD): 37 from the contralateral flocculus and 3 from the ipsilateral one. None of the neurons could be activated antidromically from both flocculi. Floccular stimulation never resulted in direct inhibition of these NPH neurons. 3. Of the 37 units antidromically activated from the contralateral flocculus, 26 were recorded sufficiently long to allow full quantitative analysis. Most of these (20 neurons) were classified as burst-tonic (BT) neurons. The BT neurons exhibited during each saccade made in one direction (the ON direction) a burst of spikes, and during postsaccadic fixation a tonic activity that increased with gaze displacement in the ON direction. The mean sensitivity of the neurons to eye velocity during the "ON" saccades was 3.3 +/- 1.6 spikes.s-1.deg-1.s-1. During intersaccadic fixation, the mean sensitivity to eye position was 3.6 +/- 2.5 spikes.s-1.deg-1. During the VOR, the majority showed modulation in relation to both eye position and eye velocity. The mean sensitivity to eye position during the VOR was 3.4 +/- 2.6 spikes.s-1.deg-1 (range: 0.2-8.1 spikes.s-1.deg-1). The mean sensitivity to eye velocity during the VOR was 2.1 +/- 1.3 spikes.s-1.deg-1.s-1. The mean phase lead of with respect to eye position was 16.4 +/- 6.8 degrees (range: 6.0-28.9 degrees). Eighty percent of the BT neurons behaved as type I neurons. Forty-seven percent of the BT neurons also presented some head velocity sensitivity (1.48 +/- 0.6 spikes.s-1.deg-1.s-1, mean +/- SD). 4. Other NPH cells antidromically activated from the contralateral flocculus were classified in two groups: bidirectional burst (BB) neurons (n = 4) and burst-driving (BD) neurons (n = 2). The BB neurons were characterized by a burst discharge during every horizontal saccade or VOR quick phase, irrespective of the direction. The mean sensitivity of the BB neurons to eye velocity during saccades was 3.3 +/- 7.8 (SD) spikes.s-1.deg-1.s-1. Both BD neurons increased their firing rate during the slow VOR phases induced by an ipsilateral rotation (type I neurons) and exhibited high-frequency bursts in association with ipsilaterally directed quick phases. 5. The results indicate that the main projection of the NPH onto the middle zone of the flocculus comes from contralaterally located type I BT neurons. Signals transmitted in this path associate a high sensitivity for eye velocity with a high sensitivity for eye position. This type of input is consistent with the suggestion that the main function of the flocculus is to control the gain of downstream reflexes and to perform a fine adjustment of the gaze holding command.

Animals↗
PubMed2005

Matrix inclusion within synthetic hydrogel guidance channels improves specific supraspinal and local axonal regeneration after complete spinal cord transection.

We have previously shown that a novel synthetic hydrogel channel composed of poly(2-hydroxyethyl methacrylate-co-methyl methacrylate) (pHEMA-MMA) is biocompatible and supports axonal regeneration after spinal cord injury. Our goal was to improve the number and type of regenerated axons within the spinal cord through the addition of different matrices and growth factors incorporated within the lumen of the channel. After complete spinal cord transection at T8, pHEMA-MMA channels, having an elastic modulus of 263+/-13 kPa were implanted into adult Sprague Dawley rats. The channels were then filled with one of the following matrices: collagen, fibrin, Matrigel, methylcellulose, or smaller pHEMA-MMA tubes placed within a larger pHEMA-MMA channel (called tubes within channels, TWC). We also supplemented selected matrices (collagen and fibrin) with neurotrophic factors, fibroblast growth factor-1 (FGF-1) and neurotrophin-3 (NT-3). After channel implantation, fibrin glue was applied to the cord-channel interface, and a duraplasty was performed with an expanded polytetrafluoroethylene (ePTFE) membrane. Controls included animals that had either complete spinal cord transection and implantation of unfilled pHEMA-MMA channels or complete spinal cord transection. Regeneration was assessed by retrograde axonal tracing with Fluoro-Gold, and immunohistochemistry with NF-200 (for total axon counts) and calcitonin gene related peptide (CGRP, for sensory axon counts) after 8 weeks survival. Fibrin, Matrigel, methylcellulose, collagen with FGF-1, collagen with NT-3, fibrin with FGF-1, and fibrin with NT-3 increased the total axon density within the channel (ANOVA, p<0.05) compared to unfilled channel controls. Only fibrin with FGF-1 decreased the sensory axon density compared to unfilled channel controls (ANOVA, p<0.05). Fibrin promoted the greatest axonal regeneration from reticular neurons, and methylcellulose promoted the greatest regeneration from vestibular and red nucleus neurons. With Matrigel, there was no axonal regeneration from brainstem motor neurons. The addition of FGF-1 increased the axonal regeneration of vestibular neurons, and the addition of NT-3 decreased the total number of axons regenerating from brainstem neurons. The fibrin and TWC showed a consistent improvement in locomotor function at both 7 and 8 weeks. Thus, the present study shows that the presence and type of matrix contained within synthetic hydrogel guidance channels affects the quantity and origin of axons that regenerate after complete spinal cord transection, and can improve functional recovery. Determining the optimum matrices and growth factors for insertion into these guidance channels will improve regeneration of the injured spinal cord.

Animals↗
PubMed1975

Physiologic characteristics of vestibular first-order canal neurons in the cat. I. Response plane determination and resting discharge characteristics.

The response plane and resting rate characteristics of first-order, vestibular, semicircular canal neurons were studied in 67 cats under sodium pentobarbital anesthesia using single-unit recording techniques in the eighth nerve. Five hundred fifty-nine units were classified as to the canal they were associated with by employing an identification technique based on physiologic response patterns to brief, high-level (up to 250 degrees/S2) angular accelerations delivered in various head positions. All horizontal canal neurons had increased firing rates to ampullopetal and all vertical canal units to ampullofugal endolymph flow. The average observed roll and pitch null points for each canal were used to determine the average sensitivity vectors for the right horizontal, anterior, and posterior canals. These sensitivity vectors were at a variance of 4.6-10.2 degrees from those predicted by anatomical measurements (3). The mean resting discharge characteristics of 318 first-order neurons was 36.0 spikes/s (range 0.50-114 spikes/s). No significant difference was noted between horizontal and anterior canal neurons on horizontal and anterior canal neurons on the basis of resting rate. The resting rate of the posterior canal neuron population was significantly lower. The regularity of the resting discharge varied in all three canals and the average coefficient of variation was 0.238 for the population, with a range of 0.298-1.030. The population distribution of all resting-rate statistical parameters appeared to be unimodal, indicating that first-order canal neurons may not be broken into discrete populations on the basis of resting-rate characteristics. Of 47 adequately examined first-order canal neurons, 25 demonstrated a repeatable and predictable alteration in their resting discharge as their position to gravity was reoriented. This alteration was usually nonadapting and varied in magnitude according to the degree of tilt and original starting position. Of 25 canal gravity units, 4 had nearby units from the same canal which were unresponsive to gravity, suggesting the effect was due to a limited distortion of the crista or cupula rather than an overall displacement of the cupula.

Acceleration↗
PubMed1980

Distribution of visual input to the vestibular nuclei.

The electrical activity of individual vestibular nuclear neurons was recorded in anesthetized and paralyzed cats and their responses to photic stimulation of the retina were studied. The visual input produced various types of unit responses. The cells of the superior vestibular nucleus showed a predominant excitatory response, the neurons of the medial vestibular nucleus displayed different combinations of excitatory and inhibitory effects, while those of the descending vestibular nucleus responded with excitation followed by inhibition. Photic stimulation of the retina elicited responses of vestibular nuclei with different latencies. The superior and medial vestibular nuclei showed shorter latencies. It is concluded tht the visual input may reach the vestibular complex thus participating in the reflex control of the ocular motoneurons.

Animals↗
PubMed1996

Synapses from medial olivocochlear branches in the inferior vestibular nucleus.

Olivocochlear neurons are auditory efferent neurons that convey information from the brainstem to the auditory periphery. With light and electron microscopy, using mice, we studied the central branches of medial olivocochlear neurons that are given off to the inferior vestibular nucleus. At the level of the electron microscope, the branches form synapses. The synapses are asymmetric with round vesicles, suggesting that they are excitatory. The synapses are formed mainly onto neuronal dendrites. These dendrites have a large range of diameters, and they may emanate from several types of target neurons. These results indicate that the inferior vestibular nucleus is an integrating center for vestibular, auditory, and other types of information, but the results do not fit with current theories about the function of the olivocochlear system.

Animals↗
PubMed1979

Vestibular nuclei activity in the alert monkey during suppression of vestibular and optokinetic nystagmus.

Single neurons were recorded in the vestibular nuclei of monkeys trained to suppress nystagmus by visual fixation during vestibular or optokinetic stimulation. During optokinetic nystagmus vestibular nuclei neurons exhibit frequency changes. With the suppression of optokinetic nystagmus this neuronal activity on average is attenuated by 40% at stimulus velocities of 40 degrees/s. At a stimulus velocity of 5 degrees/s responses are, under both conditions, close to threshold. For steps in velocity, suppression of vestibular nystagmus shortens the time constants of the decay of neuronal activity from 15--35 s to 5--9 s, while the amplitude of the response remains unchanged. The results are discussed in relation to current models of visual-vestibular interaction. These models use a feedback mechanism which normally operates during vestibular and optokinetic nystagmus. Nystagmus suppression interrupts this feedback loop.

Animals↗
PubMed1997

Neurons in rostral ventrolateral medulla mediate vestibular inhibition of locus coeruleus in rats.

The effects of caloric vestibular stimulation on the central noradrenergic neurons system were examined in the rat. In urethane-anesthetized rats, caloric stimulation inhibited the spontaneous activity of noradrenergic locus coeruleus neurons and increased systemic blood pressure. Electrical and chemical lesions in the ventrolateral medulla attenuated both the locus coeruleus inhibition and the blood pressure increase in response to caloric stimulation. Neither the neuronal inhibition nor the pressor effect was attenuated by any deafferentation of the forebrain or baroreceptors, or lesioning of the nucleus tractus solitarius. These findings indicate that the caloric stimulation-induced locus coeruleus inhibition is mediated by neurons in the ventrolateral medulla, and that these neurons also mediate the vestibulo-pressor responses. The locus coeruleus inhibition via the ventrolateral medulla is, however, considered to be independent of ventrolateral medulla-mediated systemic pressor effect. Collectively these findings suggest that the ventrolateral medulla is the major origin of inhibitory vestibular input to the noradrenergic neurons of the locus coeruleus, and that the ventrolateral medulla plays an important role in the vestibulo-autonomic response.

Animals↗
PubMedDate not supplied

Responses of hypothalamic neurons to stimulation of the vestibular nerve and lateral vestibular nucleus in the rabbit.

Acute experiments were performed on rabbits to study the responses of neurons in the anterior, ventromedial, and posterior nuclei of the hypothalamus to single, paired, and rhythmic stimulation of the vestibular nerve and lateral vestibular nucleus of Deiters. The data obtained showed that neurons of the posterior nucleus of the hypothalamus were the most sensitive. Three types of response were seen from hypothalamic neurons, with short, long, and intermediate latent periods. This provides evidence that ascending afferent spike activity from the lateral vestibular nucleus of Deiters to the hypothalamus is mediated by mono-, oligo-, and polysynaptic pathways.

Animals↗
PubMed1983

Effects of diphenhydramine iontophoretically applied onto neurons in the medial and lateral vestibular nuclei.

Electrophysiological studies were carried out to elucidate the effects of diphenhydramine, an antihistamine (H1-receptor blocking) drug, on neuron activities in the medial vestibular nucleus (MVN) and lateral vestibular nucleus (LVN) of cats using a microiontophoretic method. According to the firing pattern and latency of the first spike with vestibular nerve stimulation, neurons in the MVN and LVN were classified into two groups: monosynaptic and polysynaptic neurons. In the MVN, the spike generation of polysynaptic neurons was dose-dependently inhibited with the iontophoretic application of diphenhydramine up to 200 nA, and that of the monosynaptic neurons was also suppressed by the maximum dose of 200 nA. In contrast to the MVN neurons, the spike generation of LVN monosynaptic neurons remained unaffected with diphenhydramine up to 200 nA, although an inhibition of the LVN polysynaptic neurons was obtained with 200 nA of the drug. These results suggest that small doses of diphenhydramine more selectively interfere with synaptic transmission in the MVN neuron than that in the LVN neuron.

Animals↗