Lateral Vestibular Nucleus Neurons Research Articles

Corticotropin-releasing factor depolarizes rat lateral vestibular nuclear neurons through activation of CRF receptors 1 and 2

Corticotropin-releasing factor (CRF) is a neuropeptide mainly synthesized in the hypothalamic paraventricular nucleus and has been traditionally implicated in stress and anxiety. Intriguingly, genetic or pharmacological manipulation of CRF receptors affects locomotor activity as well as motor coordination and balance in rodents, suggesting an active involvement of the central CRFergic system in motor control. Yet little is known about the exact role of CRF in central motor structures and the underlying mechanisms. Therefore, in the present study, we focused on the effect of CRF on the lateral vestibular nucleus (LVN) in the brainstem vestibular nuclear complex, an important center directly contributing to adjustment of muscle tone for both postural maintenance and the alternative change from the extensor to the flexor phase during locomotion. The results show that CRF depolarizes and increases the firing rate of neurons in the LVN. Tetrodotoxin does not block the CRF-induced depolarization and inward current on LVN neurons, suggesting a direct postsynaptic action of the neuropeptide. The CRF-induced depolarization on LVN neurons was partly blocked by antalarmin or antisauvagine-30, selective antagonists for CRF receptors 1 (CRFR1) and 2 (CRFR2), respectively. Furthermore, combined application of antalarmin and antisauvagine-30 totally abolished the CRF-induced depolarization. Immunofluorescence results show that CRFR1 and CRFR2 are co-localized in the rat LVN. These results demonstrate that CRF excites the LVN neurons by co-activation of both CRFR1 and CRFR2, suggesting that via the direct modulation on the LVN, the central CRFergic system may actively participate in the central vestibular-mediated postural and motor control.

Histamine Increases Neuronal Excitability and Sensitivity of the Lateral Vestibular Nucleus and Promotes Motor Behaviors via HCN Channel Coupled to H2 Receptor

Histamine and histamine receptors in the central nervous system actively participate in the modulation of motor control. In clinic, histamine-related agents have traditionally been used to treat vestibular disorders. Immunohistochemical studies have revealed a distribution of histaminergic afferents in the brainstem vestibular nuclei, including the lateral vestibular nucleus (LVN), which is critical for adjustment of muscle tone and vestibular reflexes. However, the mechanisms underlying the effect of histamine on LVN neurons and the role of histamine and histaminergic afferents in the LVN in motor control are still largely unknown. Here, we show that histamine, in cellular and molecular levels, elicits the LVN neurons of rats an excitatory response, which is co-mediated by the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and K+ channels linked to H2 receptors. Blockage of HCN channels coupled to H2 receptors decreases LVN neuronal sensitivity and changes their dynamic properties. Furthermore, in behavioral level, microinjection of histamine into bilateral LVNs significantly promotes motor performances of rats on both accelerating rota-rod and balance beam. This promotion is mimicked by selective H2 receptor agonist dimaprit, and blocked by selective H2 receptor antagonist ranitidine. More importantly, blockage of HCN channels to suppress endogenous histaminergic inputs in the LVN considerably attenuates motor balance and coordination, indicating a promotion role of hypothalamo-vestibular histaminergic circuit in motor control. All these results demonstrate that histamine H2 receptors and their coupled HCN channels mediate the histamine-induced increase in excitability and sensitivity of LVN neurons and contribute to the histaminergic improvement of the LVN-related motor behaviors. The findings suggest that histamine and the histaminergic afferents may directly modulate LVN neurons and play a critical role in the central vestibular-mediated motor reflexes and behaviors.

Peripheral nerve graft with immunosuppression modifies gene expression in axotomized CNS neurons

Adult central nervous system (CNS) neurons do not regenerate severed axons unaided but may regenerate axons into apposed predegenerated peripheral nerve grafts (PNGs). We examined gene expression by using microarray technology in laser-dissected lateral vestibular (LV) neurons whose axons were severed by a lateral hemisection at C3 (HX) and in lateral vestibular nucleus (LVN) neurons that were hemisected at C3 and that received immunosuppression with cyclosporine A (CsA) and a predegenerated PNG (termed I-PNG) into the lesion site. The results provide an expression analysis of temporal changes that occur in LVN neurons in nonregenerative and potentially regenerative states and over a period of 42 days. Axotomy alone resulted in a prolonged change in regulation of probe sets, with more being upregulated than downregulated. Apposition of a PNG with immunosuppression muted gene expression overall. Axotomized neurons (HX) upregulated genes commonly associated with axonal growth, whereas axotomized neurons whose axons were apposed to the PNG showed diminished expression of many of these genes but greater expression of genes related to energy production. The results suggest that axotomized LVN neurons express many genes thought to be associated with regeneration to a greater extent than LVN neurons that are apposed to a PNG. Thus the LVN neurons remain in a regenerative state following axotomy but the conditions provided by the I-PNG appear to be neuroprotective, preserving or enhancing mitochondrial activity, which may provide required energy for regeneration. We speculate that the graft also enables sufficient axonal synthesis of cytoskeletal components to allow axonal growth without marked increase in expression of genes normally associated with regeneration.

Histamine excites rat lateral vestibular nuclear neurons through activation of post-synaptic H2 receptors

Through whole-cell patch recordings in brainstem slices, the effects of histamine on neuronal activity of the lateral vestibular nucleus (LVN) were investigated. Bath application of histamine elicited a concentration-dependent excitation of both spontaneous firing (n=19) and silent (n=7) LVN neurons. Moreover, histamine induced a stable inward current in the LVN neurons (n=5) and the histamine-induced depolarization of membrane potential persisted in the presence of tetrodotoxin (n=4), indicating a direct post-synaptic effect of the histamine on the LVN neurons. Selective histamine H2 receptor antagonist ranitidine effectively blocked the histamine-evoked excitatory responses on the LVN neurons (n=4), but selective histamine H1 receptor antagonist triprolidine did not (n=4). In addition, selective histamine H2 receptor agonist dimaprit (n=3) rather than 2-pyridylethylamine (n=4), a selective histamine H1 receptor agonist, mimicked the excitatory action of histamine on LVN neurons. The results demonstrate that histamine excites the LVN neurons via post-synaptic histamine H2 receptors and suggest that the central histaminergic projection arising from the hypothalamus may modulate LVN neurons activity and actively influence the vestibular reflexes and functions.

Noradrenaline modulates neuronal responses to GABA in vestibular nuclei

The effects of noradrenaline (NA) on the inhibitory responses to GABA were studied in vivo in neurons of the vestibular nuclei of the rat using extracellular recordings of single unit electrical activity and a microiontophoretic technique of drug application in loco. NA application influenced GABA-evoked inhibitions in 82% of tested neurons, depressing them in 42% and enhancing them in 40% of cases. The more frequent action of NA on GABA responses was depressive in lateral and superior vestibular nuclei (50% of neurons) and enhancing in the remaining nuclei (56% of neurons). The most intense effect of NA application was the enhancement of GABA responses induced in a population of lateral vestibular nucleus neurons, characterized by a background firing rate significantly higher than that of other units. The alpha2 noradrenergic receptor agonist clonidine mimicked the enhancing action of NA on GABA responses; this action was blocked by application of the specific alpha2 antagonist yohimbine. The beta adrenergic agonist isoproterenol induced either depressive or enhancing effects on GABA responses; the former more than the latter were totally or partially blocked by application of the beta antagonist timolol. It is concluded that NA enhances GABA responses by acting on noradrenergic alpha2 and to a lesser extent beta receptors, whereas depressive action involves beta receptors only.These results confirm the hypothesis that the noradrenergic system participates in the regulation of the vestibulospinal and the vestibulo-ocular reflexes and suggest that conspicuous changes of NA content in brain due to aging or stress could lead to a deterioration in the mechanisms of normal vestibular function.

Dynamics of the background impulse activity of neurons of the lateral vestibular nucleus in the norm and under vibrational influence

The background impulse activity (BIA) generated by neurons of the right lateral vestibular nucleus (LVN) of rats in the norm and under conditions of long-lasting general vibrational stimulation was subjected to computer analysis. Statistically significant changes in intragroup values of the mean BIA frequency were observed after 5 and 10 days with 2-h-long sessions of vibrational stimulation. Significant shifts in the distributions of LVN neurons by the level of regularity and dynamic types of BIA were observed 10 and 15 days with vibrational influences. Trends toward return of the intragroup mean value of the BIA frequency to the initial level were noticeable at the end of the stimulation period (15 days).

Input/output properties of the lateral vestibular nucleus.

This article is a review of work in three species, squirrel monkey, cat, and rat studying the inputs and outputs from the lateral vestibular nucleus (LVN). Different electrophysiological shock paradigms were used to determine the synaptic inputs derived from thick to thin diameter vestibular nerve afferents. Angular and linear mechanical stimulations were used to activate and study the combined and individual contribution of inner ear organs and neck afferents. The spatio-temporal properties of LVN neurons in the decerebrated rat were studied in response to dynamic acceleration inputs using sinusoidal linear translation in the horizontal head plane. Outputs were evaluated using antidromic identification techniques and identified LVN neurons were intracellularly injected with biocytin and their morphology studied.

Morphological study of the space distribution of vestibulospinal neurons in the frog Rana ridibunda

In the thew frog Rana ridibunda, local microphoretic injections of horseradish peroxidase into various parts of spinal cord were used for study of trajectory of retrograde enzyme-labeled fiber systems and topography of labeled neurons in vestibulospinal nuclei, the source of vestibulospinal fibers. The vestibulospinal tracts were shown to be formed by neurons of lateral vestibular nucleus, although descending vestibular nucleus also is partially involved, while medial vestibular nucleus contributes to even lesser degree. Besides, study of spatial distribution of C- and L-vestibulospinal neurons in the frog did not confirm the presence of the definite somatotopy that is characteristic of vestibular nuclei in mammals.

Expression of c-jun in the lateral vestibular nucleus following spinal cord injury and peripheral nerve graft transplantation in adult rats.

The time course of c-jun expression and the effect of a peripheral nerve (PN) graft on axonal regeneration and c-jun expression in the lateral vestibular nucleus (LVN) were investigated in this study. c-Jun was found in LVN neurons 1 day after hemisection of the spinal cord at C3, with weak immunoreactivity. Strong c-Jun positive immunoreactivity was found 3 days post-injury. The expression of c-jun reached its maximum level (45% +/- 2.5, mean +/- SD) 1 week post-injury and gradually decreased to about a third of its peak value 6 weeks after the inflicted lesion. The PN graft implanted at the lesion site significantly enhanced the number of neurons expressing c-jun 4 weeks after PN transplantation (from 20% of LVN neurons in axotomy alone to 30% in PN graft transplantation, P < 0. 05). The PN graft induced injured neurons to regrow into the PN graft. About 91 FG-labeled neurons were found in the LVN and approximately 87% of these neurons showed c-Jun positive immunoreactivity. The high percentage of regenerating neurons expressing c-jun suggested that c-Jun might be involved in the regenerative process. The result of double staining for c-Jun and NOS showed that approximately 93% NOS positive neurons co-expressed c-Jun. Comparing the time course of the appearance of c-Jun with that of NOS, the expression of c-jun preceded that of NOS. Although a high percentage of NOS reactive neurons expressed c-jun, the expression of NOS in damaged LVN neurons needs to be further investigated.

5-HT 1A receptor-mediated inhibition of lateral vestibular nucleus neurons projecting to the abducens nucleus

Electrophysiological studies were performed using cats anesthetized with α-chloralose, to elucidate the 5-hydroxytryptamine (5-HT) receptor subtypes involved in the 5-HT-induced inhibition of the lateral vestibular nucleus (LVN) neurons projecting to or through the abducens nucleus. The effects of 5-HT receptor subtype agonists and antagonist were examined in polysynaptic neurons activated by stimulation of the ipsilateral abducens nucleus (IAN) antidromically, since these neurons are sensitive to 5-HT as shown in our previous study. Iontophoretic application of 5-HT and8-hydroxy-2-(di- n-propylamino)tetrain (8-OH-DPAT), a selective 5-HT 1A agonist, inhibited orthodromic spikes elicited by vestibular nerve stimulation in the majority of polysynaptic neurons activated by stimulation of ipsilateral IAN antidromically. There was a good correlation between the effects of 5-HT and 8-OH-DPAT. Iontophoretically applied 5-HT and 8-OH-DPAT also inhibited glutamate-induced firing in these neurons. Simultaneous application of 1-(2-methoxyphenly)-4-[4-(2-phthalimido)butyl]piperazine (NAN-190), a 5-HT 1A agonist/antagonist, significantly antagonized the 8-OH-DPAT-induced inhibition of glutamate-induced firing, although NAN-190 alone also caused weak suppression of glutamate-induced firing. Microiontophoretically applied 1-(3-chlorophenyl)piperazine (mCPP), a 5-HT 1B agonist inhibited the orthodromic spike elicited by vestibular nerve stimulation and glutamate-induced firing in only a small number of the LVN neurons. 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a 5-HT 2 agonist, rarely affected these neurons. We postulate that postsynaptically located 5-HT 1A receptors are mainly involved in the 5-HT-induced inhibition of polysynaptic neurons projecting in the region of the IAN.

Temporal response properties of lumbar-projecting vestibulospinal neurons to roll tilt in decerebrate cats

In decerebrate cats, rotation about the longitudinal axis of the animal, leading to sinusoidal stimulation of labyrinth receptors, produces a tonic contraction of limb extensors during side-down tilt (alpha responses) and of dorsal neck extensors during side-up tilt (beta responses). These changes in posture are mediated, at least in part, by lateral vestibular nucleus (LVN) neurons, with response characteristics to stimulation of macular and/or canal receptors that have so far been evaluated at the level of either unidentified vestibulospinal (VS) neurons or vestibulo-collic neurons projecting to the upper cervical cord. In the present study we investigated the dynamics of the responses of VS neurons projecting to the lumbosacral segments of the spinal cord to increasing frequencies of tilt (from 0.026 to 0.32 Hz, +/- 10 degrees). All the recorded units showed an average phase lead with respect to position of +25.6 +/- 5.5 degrees (SE) at the tilt frequency of 0.026 Hz. Most of these neurons (n = 32) were particularly activated during side-down tilt (alpha responses) and showed either a stable phase or an increase in phase lead of the responses with increasing frequency of tilt. At the tilt frequency of 0.026 Hz, the smaller the phase lead of the responses, the larger was the response gain. Moreover, the smaller the phase lead of the responses at that frequency of tilt, the smaller the increase in gain but the larger was the increase in lead of the responses obtained by increasing the stimulation frequency up to 0.32 Hz. Through this set of finely organized changes in unit response characteristics, the overall output of this population of neurons increased, while the phase angle of the responses reached the mean value of +64.9 +/- 2.6 degrees (SE), thus becoming more related to the velocity than to the positional signal. The remaining units (n = 7), which were mainly activated during side-up tilt (beta responses), displayed an increase in phase lag of the responses to increasing frequency of stimulation, which reached the mean value of -118.9 +/- 14.5 degrees (SE) at 0.32 Hz. The differences in the dynamic properties of these VS neurons projecting to the lumbosacral cord, with respect to those of previously recorded populations of VS neurons, are discussed.

Activity of lateral vestibular nucleus neurons during locomotion in the decerebrate guinea pig.

The influence of locomotor activity upon neurons in the lateral vestibular nucleus was investigated in precollicularly-postmamillary decerebrate guinea pigs. Out of 95 recorded neurons, 24 were identified as vestibulospinal and 71 had no descending projections. Locomotor activity occurred either spontaneously or was prompted by electrical stimulation of the mesencephalic locomotor region. Natural vestibular stimulation was supplied by tilting the animal about its longitudinal axis. Locomotor rhythmic limb muscle activity was accompanied by an increase in the firing frequency in the vast majority of investigated neurons. The increase in frequency was observed at the beginning of ipsilateral forelimb extensor muscle activity. Only in a few non-vestibulospinal neurons was the spontaneous activity depressed during locomotion. An increase in evoked responses was observed in almost all vestibulospinal neurons and in two thirds of the neurons without descending projections. A decrease in evoked responses was observed in one quarter of non-vestibulospinal neurons. During locomotion, the mean and maximal frequencies of evoked neuronal impulse activity changed, but the phase lag of these changes was not altered significantly. The results suggest an enhancement of vestibulospinal influences during locomotion, thus providing a high level of tonus in antigravitational muscles. This is interpreted as a mechanism to ensure that equilibrium is maintained during motion in different gaits and postures.

Inhibition of lateral vestibular nucleus neurons by 5-hydroxytryptamine derived from the dorsal raphe nucleus

Electrophysiological studies were performed to elucidate the effect of 5-hydroxytryptamine (5-HT) originating in the dorsal raphe nucleus (DR) on neuronal activity in the lateral vestibular nucleus (LVN) neurons, using cats anesthetized with α-chloralose. LVN neurons were classified into monosynaptic and polysynaptic neurons according to their responses to vestibular nerve stimulation. Conditioning stimuli applied to the DR inhibited orthodromic spikes elicited by vestibular nerve stimulation predominantly in polysynaptic neurons of the LVN. The iontophoretic application of 5-HT also inhibited orthodromic spikes of the LVN neurons. A close correlation was observed between the effects of DR conditioning stimulation and iontophoretically applied 5-HT in the same neurons. These inhibitions with both treatments were antagonized during the application of methysergide, a 5-HT antagonist. In the majority of LVN polysynaptic neurons that responded to antidromic stimulation of the ipsilateral or contralateral abducens nucleus, orthodromic spikes elicited by vestibular nerve stimulation were inhibited by DR conditioning stimulation and the iontophoretic application of 5-HT. In contrast, LVN neurons that responded to antidromic stimulation of the vestibulospinal tract were rarely affected by these treatments. These results indicate that 5-HT derived from the DR inhibits the synaptic transmission of LVN polysynaptic neurons ascending to the abducens nucleus, and suggest that 5-HT derived from the DR is involved in the regulation of the vestibulo-ocular reflex.

Responses and Anatomical Connections of Peripheral Vestibular Neurons Innervating Otolith Organs

The response patterns of the Scarpa's neurons and lateral vestibular nucleus (LVN) neurons that respond to lateral and antero-posterior tilting were investigated using cats. The following observations were made: 1) The Scarpa's neurons that respond to lateral tilting have directional sensitivity physiologically and may innervate the utricular macula; 2) The LVN neurons that respond to lateral tilting are found mostly in the ventral part of the LVN and also have directional sensitivity. They project toward the spinal cord into the lateral vestibulo-spinal tract.

P-008 - Inhibition of lateral vestibular nucleus neurons by 5-hydroxytryptamine derived from the dorsal raphe nucleus

Abstract Electrophysiological studies were performed to elucidate the effect of 5-hydroxytryptamine (5-HT) originating in the dorsal raphe nucleus (DR) on neuronal activity in the lateral vestibular nucleus (LVN) neurons, using cats anesthetized with α-chloralose. LVN neurons were classified into monosynaptic and polysynaptic neurons according to their responses to vestibular nerve stimulation. Conditioning stimuli applied to the DR inhibited orthodromic spikes elicited by vestibular nerve stimulation predominantly in polysynaptic neurons of the LVN. The iontophoretic application of 5-HT also inhibited orthodromic spikes of the LVN neurons. A close correlation was observed between the effects of DR conditioning stimulation and iontophoretically applied 5-HT in the same neurons. These inhibitions with both treatments were antagonized during the application of methysergide, a 5-HT antagonist. In the majority of LVN polysynaptic neurons that responded to antidromic stimulation of the ipsilateral or contralateral abducens nucleus, orthodromic spikes elicited by vestibular nerve stimulation were inhibited by DR conditioning stimulation and the iontophoretic application of 5-HT. In contrast, LVN neurons that responded to antidromic stimulation of the vestibulospinal tract were rarely affected by these treatments. These results indicate that 5-HT derived from the DR inhibits the synaptic transmission of LVN polysynaptic neurons ascending to the abducens nucleus, and suggest that 5-HT derived from the DR is involved in the regulation of the vestibulo-ocular reflex.

中耳圧の前庭神経外側核ニューロン活動に及ぼす影響

We have reported that middle ear pressure changes influenced vestibular nerve activity. In the present study the influence of middle ear pressure on the lateral vestibular nucleus neurons was investigated in anesthetized cats. The activities of the lateral vestibular nucleus neurons, especially the lateral vestibulo-spinal tract neurons, were recorded extracellularly. Positive or negative pressure was applied to the middle ear cavity bilaterally through perforation of the tympanic membrane.In most lateral vestibular nucleus neurons firings were increased with negative pressure and decreased with positive pressure. These effects were more prominent when pressure changes were applied to the contralateral middle ear cavity. These influences of middle ear pressure on the lateral vestibular nucleus neurons were opposite to those on the vestibular nerve, and the existence of inhibitory interneurons was considered.

Effects of motor cortex and single muscle stimulation on neurons of the lateral vestibular nucleus in the rat

The neuronal responses to stimulation of motor cortical sites and of forelimb single muscles were studied in the lateral vestibular nucleus of anaesthetized rats. Of the 228 neurons tested for response to stimulation of contralateral motor cortex, 63% responded to cortical sites controlling extensor muscles and 30% to those controlling flexors. The corresponding figures for responders to ipsilateral stimulation were 34 and 21%. Vestibulospinal units responded to cortical sites controlling extensor and flexor muscles whereas the remaining lateral vestibular nucleus neurons, very reactive to cortical sites controlling extensor muscles, responded little to contralateral and not at all to ipsilateral cortical sites controlling flexor muscles. The effects evoked by contralateral cortical sites controlling extensors varied, those induced by cortical sites controlling flexors were inhibitory in 77% of cases. The responses to ipsilateral motor cortex stimulation differed not so much by cortical sites controlling extensor or flexor muscles as by whether the neuron was in the dorsal or ventral zone of the lateral vestibular nucleus: mixed in the former, all inhibitory in the latter. Of the lateral vestibular nucleus units tested for response to stimulation of ipsilateral or contralateral forelimb distal muscles, only 11% responded. All the vestibulospinal units responsive to muscle stimulation lay in the dorsal zone of the nucleus. The remainder, dorsal or ventral, were not responsive to contralateral muscles. Single lateral vestibular nucleus cells influenced both by ipsilateral muscle and by contralateral motor cortex made up 24% of the pool, vestibulospinal and non-vestibulospinal. They fell into three groups: responsive to one or both structures but responding more strongly to combined stimulation; responsive to each of the two structures but showing a response to combined stimulation not significantly different from that evoked by the cortex alone; responsive only to combined stimulation. The lateral vestibular nucleus units included in these three groups accounted for 29% of those tested for response to extensor muscles and cortical sites controlling extensors and 15% of those tested for response to flexor muscles and cortical sites controlling flexors. Twenty-five per cent of the vestibulospinal neurons responded both to contralateral muscles and to ipsilateral motor cortex stimulation but none of the non-vestibulospinal neurons responded to both. All the responders to both were in the dorsal zone of the lateral vestibular nucleus and responded to extensor stimuli, always in the same way. These results indicate that motor cortex output exerts a major influence on lateral vestibular nucleus discharges, while the muscle afferents have a modulatory influence on the lateral vestibular nucleus responses to cortex. The units more responsible for integration of cortical and peripheral information are the vestibulospinal neurons of the dorsal zone.

The lateral vestibular nucleus is a site for the depressant action of benzodiazepines on the crossed extensor reflex

The effects of diazepam microinjected into the subcerebellar nuclei, the lateral vestibular nucleus (LVN), the red nucleus and the substantia nigra were investigated using the crossed extensor reflex (CER) model in chloralose-anesthetized rats. Microinjections of diazepam at doses of 1 and 25 ng/animal into the left LVN, ipsilateral to the testing muscle, produced a dose-related CER depression, while injections of diazepam at a dose of up to 100 ng/animal into the right LVN and into other regions tested produced little effect. The CER depression produced by diazepam could be clearly reversed by a subsequent intravenous administration of Ro 15-1788, a benzodiazepine antagonist. Electrical lesions of the left LVN decreased the amplitude of CER in otherwise untreated rats. Intravenously administered diazepam at a dose of 0.01 or 0.05 mg/kg decreased spontaneous firing of LVN neurons. Iontophoretically applied GABA or flurazepam, a water-soluble benzodiazepine, decreased the spontaneous firing of LVN neurons. Depressant actions on neuronal activity in the LVN produced by both diazepam and flurazepam were clearly antagonized by intravenously administered Ro 15-1788, while it failed to reverse the depression produced by GABA. These findings indicate that the LVN is a major site of the CER depressant action of benzodiazepines and a possible mechanism of action is discussed.

Different sensitivity to hypoxia in neuronal activities of lateral vestibular and spinal trigeminal nuclei.

Electrophysiologic studies were performed to examine the effects of hypoxia on neuronal activities of the lateral vestibular and spinal trigeminal nuclei using rats anesthetized with chloral hydrate. The rats inhaled a gas mixture of 5% oxygen and 95% nitrogen for 3.5 minutes to induce hypoxia, followed by room air. Under these conditions, mean PaO2 was decreased from 85 to 22 mm Hg 3 minutes after the start of the inhalation concomitant with a decrease in blood pressure from 108 to 55 mm Hg. There were no significant differences in these variables between rats used for vestibular nucleus experiments and rats used for trigeminal nucleus experiments. In the lateral vestibular nucleus, hypoxia inhibited postsynaptic components of the evoked field potential, spike generation of monosynaptic neurons on vestibular nerve stimulation, and firing induced by iontophoretic application of glutamate. In the spinal trigeminal nucleus, however, there were no alterations of the field potential or spike generation of the neurons on trigeminal nerve stimulation. These results indicate that the lateral vestibular nucleus neurons are much more sensitive to hypoxia than the spinal trigeminal nucleus neurons. The failure of transmission in the monosynaptic neurons of the lateral vestibular nucleus is suggested to be due to the inhibition of excitability of the postsynaptic membrane.

Effects of stimulation of vestibular and neck receptors on Deiters neurons projecting to the lumbosacral cord.

The activity of lateral vestibular nucleus (LVN) neurons, antidromically identified by stimulation of the spinal cord at T12 and L1, thus projecting to the lumbosacral segments of the spinal cord (IVS neurons), was recorded in precollicular decerebrate cats during rotation about the longitudinal axis either of the whole animal (labyrinth input) or of the body only while the head was kept stationary (neck input). Among the IVS neurons tested for vestibular stimulation, 76 of 129 units (i.e. 58.9%) responded to roll tilt of the animal at the standard parameters of 0.026 Hz, +/- 10 degrees. The gain and the sensitivity of the first harmonic responses corresponded on the average to 0.47 +/- 0.44, SD, impulses X s-1 X deg-1 and 3.24 +/- 3.15, SD, %/deg, respectively. As to the response patterns, 51 of 76 units (i.e. 67.1%) were excited during side-down and depressed during side-up tilt, whereas 15 (i.e. 19.7%) showed the opposite behavior. In both instances the peak of the responses occurred with an average phase lead of about +21.0 +/- 27.2, SD, deg with respect to the extreme side-down or side-up position of the animal. Moreover, the former group of units showed almost a twofold larger gain with respect to the latter group (t-test, p less than 0.05). Among the IVS neurons tested for neck stimulation, 75 of 109 units (68.8%) responded to neck rotation at the standard parameters. The gain and the sensitivity of the first harmonic responses corresponded on the average to 0.49 +/- 0.40, SD, impulses X s-1 X deg-1 and 3.30 +/- 3.42, SD, %/deg, respectively, thus being similar to the values obtained for the labyrinth responses. However, 59 of 75 units (i.e. 78.6%) were excited during side-up neck rotation and depressed during side-down neck rotation, while 8 of 75 units (i.e. 10.7%) showed the opposite pattern. In both instances the peak of the responses occurred with an average phase lead of +52.0 +/- 18.3, SD, deg for the extreme side-up or side-down neck displacements. Further, the former group of units showed a larger gain than the latter group. Histological controls indicated that 102 of 129 (i.e. 79.0%) IVS neurons tested for labyrinth stimulation and 86 of 109 (i.e. 78.9%) IVS neurons tested for neck stimulation were located in the dorsocaudal part of LVN, the remaining IVS neurons being located in the rostroventral part of LVN.(ABSTRACT TRUNCATED AT 400 WORDS)