Contralateral Medial Vestibular Nucleus Research Articles

Parvalbumin-positive neurons in the medial vestibular nucleus contribute to vestibular compensation through commissural inhibition.

The commissural inhibitory system between the bilateral medial vestibular nucleus (MVN) plays a key role in vestibular compensation. Calcium-binding protein parvalbumin (PV) is expressed in MVN GABAergic neurons. Whether these neurons are involved in vestibular compensation is still unknown. After unilateral labyrinthectomy (UL), we measured the activity of MVN PV neurons by in vivo calcium imaging, and observed the projection of MVN PV neurons by retrograde neural tracing. After regulating PV neurons' activity by chemogenetic technique, the effects on vestibular compensation were evaluated by behavior analysis. We found PV expression and the activity of PV neurons in contralateral but not ipsilateral MVN increased 6 h following UL. ErbB4 is required to maintain GABA release for PV neurons, conditional knockout ErbB4 from PV neurons promoted vestibular compensation. Further investigation showed that vestibular compensation could be promoted by chemogenetic inhibition of contralateral MVN or activation of ipsilateral MVN PV neurons. Additional neural tracing study revealed that considerable MVN PV neurons were projecting to the opposite side of MVN, and that activating the ipsilateral MVN PV neurons projecting to contralateral MVN can promote vestibular compensation. Contralateral MVN PV neuron activation after UL is detrimental to vestibular compensation, and rebalancing bilateral MVN PV neuron activity can promote vestibular compensation, via commissural inhibition from the ipsilateral MVN PV neurons. Our findings provide a new understanding of vestibular compensation at the neural circuitry level and a novel potential therapeutic target for vestibular disorders.

Effects of Betahistine on the Development of Vestibular Compensation after Unilateral Labyrinthectomy in Rats.

Background: Vestibular compensation (VC) after unilateral labyrinthectomy (UL) consists of the initial and late processes. These processes can be evaluated based on the decline in the frequency of spontaneous nystagmus (SN) and the number of MK801-induced Fos-positive neurons in the contralateral medial vestibular nucleus (contra-MVe) in rats. Histamine H3 receptors (H3R) are reported to be involved in the development of VC. Objective: We examined the effects of betahistine, an H3R antagonist, on the initial and late processes of VC in UL rats. Methods: Betahistine dihydrochloride was continuously administered to the UL rats at doses of 100 and 200 mg/kg/day using an osmotic minipump. MK801 (1.0 mg/kg) was intraperitoneally administered on days 7, 10, 12, and 14 after UL, while Fos-positive neurons were immunohistochemically stained in the contra-MVe. Results: The SN disappeared after 42 h, and continuous infusion of betahistine did not change the decline in the frequency of SN. The number of MK801-induced Fos-positive neurons in contra-MVe significantly decreased on days 7, 10, and 12 after UL in a dose-dependent manner in the betahistine-treated rats, more so than in the saline-treated rats. Conclusion: These findings suggest that betahistine facilitated the late, but not the initial, process of VC in UL rats.

Reader response: Impaired vestibular responses in internuclear ophthalmoplegia: Association and dissociation.

I read with interest the investigation of vestibular responses in internuclear ophthalmoplegia (INO) by Choi et al.1 While the data are robust, I am concerned that the explanations do not conform with prior reports. Similar to Choi et al., my colleagues and I studied initial horizontal vestibulo-ocular reflex (VOR) in 6 patients with INO and showed reduced VOR gains for both adduction and abduction.2 Because the horizontal VOR pathway is crossed, low contralesional VOR gain is attributable to damage to fibers of passage between contralateral medial vestibular nucleus and ipsilateral abducens nucleus, without implicating deranged signals from posterior canals. Similarly, adaptation to adduction paresis refers to pulse-step mismatch of abducting saccades and cannot explain reduced contralesional horizontal VOR.3 In our study,2 horizontal VOR latencies were normal, implying integrity of direct VOR. Undamaged fibers in medial longitudinal fasciculus (MLF) or extrafascicular pathways can still initiate the VOR without delay, albeit at lower gain. Variability in horizontal VOR gain is due to the extent of MLF damage. If the same premise is applied to the vertical system, posterior canal signals in the MLF would be variably affected. Ipsilesional anterior canal excitation is preserved because signals are extrafascicular. Damage to inhibitory pathways carrying disfacilitation signals in the MLF would not contribute to preserved ipsilesional or reduced contralesional anterior canal VOR.4

Changes of some amino acid concentrations in the medial vestibular nucleus of conscious rats following acute hypotension

Microdialysis and high performance liquid chromatography (HPLC) were used to measure the changes of certain amino acids in the medial vestibular nucleus (MVN) of conscious rats in order to understand whether those amino acids are involved in the regulation of blood pressure. Acute hypotension was induced by infusing sodium nitroprusside (SNP) into the femoral vein. In the control group, glutamate (Glu) release increased, though γ-aminobutyric acid (GABA) and taurine (Tau) release decreased in the MVN following acute hypotension. In the unilateral labyrinthectomy group, the levels of Glu, GABA, and Tau were unchanged in the ipsilateral MVN to the lesion following acute hypotension. Furthermore, in the contralateral MVN to the lesion, Glu release increased, and GABA and Tau release decreased following acute hypotension. These results suggest that SNP-induced acute hypotension can influence the activity of neurons in the MVN through afferent signals from peripheral vestibular receptors, and that certain amino acid transmitters in the MVN are involved in this process.

Effect of baclofen on neuronal activity in the medial vestibular nucleus after unilateral surgical labyrinthectomy in rats

Conclusions: Ipsilateral and contralateral medial vestibular nuclei (MVN) neurons respond differently to systemic injection of baclofen (4-amino-3-(4-chlorophenyl)-butanoic acid), illustrating the plastic changes of the type B γ-aminobutyric acid (GABAB) receptor during vestibular compensation. Objectives: To investigate the responsiveness of MVN neurons to baclofen during the early, partially compensated period after unilateral surgical labyrinthectomy. Materials and methods: MVN were localized using field potentials evoked by electrical stimulation, along with a stereotaxic atlas of rat brain. Neuronal activity in MVN was recorded and analyzed in rats that had undergone labyrinthectomy with and without administration of baclofen. Results: After left labyrinthectomy the mean discharge rate in ipsilesional MVN decreased, but it was nearly restored by postoperative day 8. Baclofen (3 mg/kg) reversed the mean discharge rates between bilateral MVN at days 4 and 8 after surgical labyrinthectomy. In addition, the reduction ratio of the right MVN neurons was higher than that of the left MVN neurons.

Temporal Changes of the Calcium-binding Proteins in the Medial Vestibular Nucleus following Unilateral Labyrinthectomy in Rats

Calcium (Ca(2+)) is an intracellular second messenger associated with neuronal plasticity of the central nervous system. The calcium-binding proteins regulate the Ca(2+)-mediated signals in the cytoplasm and buffer the calcium concentration. This study examined temporal changes of three calcium-binding proteins (calretinin, calbindin and parvalbumin) in the medial vestibular nucleus (MVN) during vestibular compensation after unilateral labyrinthectomy (UL) in rats. Rats underwent UL, and the changes in the expression of these proteins at 2, 6, 12, 24, 48, and 72 h were examined by immunofluorescence staining. The expression levels of all three proteins increased immediately after UL and returned to the control level by 48 h. However, the level of calretinin showed changes different from the other two proteins, being expressed at significantly higher level in the contralateral MVN than in the ipsilateral MVN 2 h after UL, whereas the other two proteins showed similar expression levels in both the ipsilateral and contralateral MVN. These results suggest that the calcium binding proteins have some protective activity against the increased Ca(2+) levels in the MVN. In particular, calretinin might be more responsive to neuronal activity than calbindin or parvalbumin.

Unilateral labyrinthectomy induced changes on GDNF receptor complex proteins in the rat medial vestibular nuclei

In the auditory periphery, GDNF has been shown to have a trophic effect to spiral ganglion neurons, both during development and in adult animals. We have studied the effect of unilateral labyrinthectomy (UL) on protein levels and expression of GDNF multicomponent receptor complex: the ret tyrosine kinase and coreceptor GFRalpha-1 in the medial vestibular nucleus of the adult rat. GFRalpha-1 protein levels display an increasing trend in ipsilateral medial vestibular nucleus culminating at 48 h post UL. On the other hand, GFRalpha-1 mRNA expression levels in ipsi- and contralateral medial vestibular nucleus show a steadily decreasing trend that is significant at 1 week post-lesion. Protein levels for c-Ret isoforms also show an initial bilateral decreasing trend that ceases at 48 h in ipsilateral medial vestibular nucleus but persists on the contralateral side. c-Ret mRNA expression levels show a significant decrease at 4 h post UL followed by another significant decrease 1 week post UL. Our data would suggest that neurotrophins belonging to the GDNF family are involved in this model of post-lesional CNS plasticity.

Anterograde tracing of projections from the dorsal raphe nucleus to the vestibular nuclei

This study used the anterograde transport of biotinylated dextran amine (BDA) to identify the course and terminal distribution of projections from the dorsal raphe nucleus (DRN) to the vestibular nuclei in rats. After iontophoretic injection of BDA into the medial and lateral regions of DRN, anterogradely labeled fibers descend within the medial longitudinal fasciculus and the ventricular fiber plexus to terminate within two discrete regions of the vestibular nuclear complex. One terminal field was located primarily ipsilateral to the injection site and involved rostrodorsal aspects of the vestibular nuclei, including superior vestibular nucleus and rostral portions of the medial vestibular nucleus (MVN) and lateral vestibular nucleus (LVN). The other terminal field involved caudoventral aspects of both ipsilateral and contralateral MVN and LVN and was less heavily innervated. These findings confirm that the vestibular nuclei are targeted by a regionally-selective projection from the DRN. The segregation of DRN terminals into anatomically distinct fields indicates that the DRN-vestibular nucleus projections are organized to selectively modulate processing within specific functional domains of the vestibular nuclear complex. In particular, these terminal fields may be organized to modulate vestibular regions involved in eye movement–related velocity storage, coordination of vestibular and affective responses, and the bilateral coordination of horizontal eye movement reflexes.

Immunocytochemical and stereological study of glucocorticoid receptors in rat medial vestibular nucleus neurons and the effects of unilateral vestibular deafferentation

Conclusion. The results of this study suggest that neither the number of medial vestibular nucleus (MVN) neurons expressing cytosolic glucocorticoid receptors nor blood corticosterone levels change significantly during the development of vestibular compensation. Objective. Vestibular compensation is a process of partial behavioral recovery that occurs following damage to the vestibular labyrinth. It has been suggested that this compensation process might be dependent on the release of glucocorticoids such as corticosterone at the time of unilateral vestibular deafferentation (UVD) and that changes in glucocorticoid receptors in the MVN might contribute to the initiation of the compensation process. Material and methods. We compared the number of MVN neurons expressing cytosolic glucocorticoid receptors in rats at 10 h and 2 weeks following UVD, and in sham and anesthetic control animals; we also measured blood corticosterone levels. Results. Using immunocytochemistry and stereology, we found that the majority of MVN neurons expressed glucocorticoid receptors, but there were no significant differences in the number of glucocorticoid receptor-expressing neurons in the ipsilateral or contralateral MVNs at 10 h or 2 weeks post-UVD; furthermore, corticosterone levels did not vary significantly between the UVD and control groups.

Temporal changes of cFos-like protein expression in medial vestibular nuclei following arsanilate-induced unilateral labyrinthectomy in rats

The compensation of spontaneous nystagmus and head deviation following chemical unilateral labyrinthectomy (UL) induced by arsanilate was delayed compared with surgical UL. Surgical UL produced two phases of significant asymmetry of cFos-like (cFL) protein expression between the bilateral medial vestibular nuclei, with more expression in the contralateral medial vestibular nuclei to the injured side than in the ipsilateral medial vestibular nuclei 2 h after UL; the pattern reversed after 6 h and expression disappeared after 72 h. Chemical UL produced three phases of asymmetric expression, with more cFL protein expression in the contralateral medial vestibular nuclei than in the ipsilateral medial vestibular nuclei 6 h after UL and a reversed pattern after 12 h. Asymmetric expression 72 h after UL followed increased expression in the contralateral medial vestibular nuclei. These results suggest that the course of vestibular compensation and the temporal expression of cFL protein in the medial vestibular nuclei following UL differed between surgical and chemical labyrinthectomy.

The effects of l-NAME on vestibular compensation and NOS activity in the vestibular nucleus, cerebellum and cortex of the guinea pig

Nitric oxide (NO) has been implicated in the processes by which animals recover from peripheral vestibular damage (‘vestibular compensation’). However, few data exist on the dose–response effects of systemic administration of the nitric oxide synthase (NOS) inhibitor, N G-nitro- l-arginine methyl ester ( l-NAME), on the vestibular compensation process. The aim of this study was to investigate the effects on compensation of 5, 10, 50 or 100 mM l-NAME administered by s.c osmotic minipump for 50 h following unilateral vestibular deafferentation (UVD) in guinea pig, either commencing the drug treatment at 4 h pre-UVD or at the time of the UVD (i.e., post-UVD). Post-UVD treatment with l-NAME, at any of the four concentrations used, had no effect on the compensation of spontaneous nystagmus (SN), yaw head tilt (YHT) or roll head tilt (RHT). By contrast, pre-UVD treatment with 100 mM l-NAME resulted in a significant decrease in SN frequency ( P<0.05) and a change in the rate of its compensation ( P<0.0005). Pre-UVD l-NAME resulted in a significant increase in the overall magnitude of YHT ( P<0.005); however, post-hoc comparisons revealed no significant differences between any specific l-NAME and vehicle groups. Pre-UVD l-NAME had no effect on RHT at any concentration. Analysis of NOS activity in the pre-UVD l-NAME treatment groups at 50 h post-UVD showed that only 100 mM l-NAME resulted in a significant decrease in NOS activity in the contralateral medial vestibular nucleus (MVN)/prepositus hypoglossi (PH) ( P<0.05) and that NOS activity in the ipsilateral MVN/PH was not significantly affected. However, NOS activity was significantly inhibited in the bilateral cerebellum and cortices for several concentrations of l-NAME. These results suggest that pre-UVD systemic administration of l-NAME can significantly increase the rate of SN compensation in guinea pig and that this effect is correlated with inhibition of NOS activity in several regions of the CNS.

Comparison of protein kinase activity and protein phosphorylation in the medial vestibular nucleus and prepositus hypoglossi in labyrinthine-intact and labyrinthectomized guinea pigs

The aim of the present study was to compare in vitro protein expression, protein kinase activity and protein phosphorylation in the medial vestibular nucleus (MVN) and prepositus hypoglossi (PH) from labyrinthine-intact guinea pigs and from guinea pigs at various stages of vestibular compensation following unilateral labyrinthectomy (UL). The ipsilateral (I-MVN) and contralateral (C-MVN) MVN, and the ipsilateral (I-PH) and contralateral (C-PH) PH, were dissected from 3 naive labyrinthine-intact guinea pigs and 55 guinea pigs at 10 hs or 53 hs following a surgical UL or sham operation. Tissue extracts were incubated with [gamma-33P]ATP+/-Ca2+, phorbol 12, 13 dibutyrate and phosphatidylserine or +/- Ca2+ and calmodulin, to enhance protein kinase C (PKC) or calcium calmodulin kinase (CaMK) activity, respectively. Data were analysed as the ratio of activated to basal 33P incorporation detected by phosphorimaging. There were similar total protein and phosphoprotein profiles in the MVN and PH, as well as both PKC and CaMKII activity, suggesting that the MVN and PH are similar in the way that proteins undergo rapid modification by phosphorylation. During the development of vestibular compensation, a 46 kDa band in C-PH displayed higher PKC-mediated phosphorylation from 10 hs post-UL compared to sham controls. Significantly greater PKC-mediated phosphorylation of proteins of approximately 18, 46 and 75 kDa was observed in C-PH at 10 hs compared to 53 hs post-UL and in most cases the phosphorylation was greater in C-PH than in the C-MVN. These results suggest that between 10 and 53 hs post-UL, PKC-mediated phosphorylation changes mainly in the C-PH rather than the ipsilateral or contralateral MVN.

Effect of MK801 on cFos-like protein expression in the medial vestibular nucleus at early stage of vestibular compensation in uvulonodullectomized rats

The purpose of this study was to evaluate the effect of uvulonodullectomy (UNL) on the expression of cFos-like protein (FLP) in the medial vestibular nucleus (MVe) during vestibular compensation and effect of MK801, an N-methyl- d-aspartate (NMDA) antagonist, on FLP expression in the brain stem nuclei at 6 h after unilateral labyrinthectomy (ULX) with UNL in Sprague–Dawley rats. Immunohistochemical staining was performed to visualize FLP in the brain stem nuclei and FLP-positive cells were counted by image analyzer. Lesion-induced asymmetric expression of FLP in the bilateral MVe was observed and maintained up to for 72 h in the ULX group, and 120 h in the UNL+ULX group. Moreover, spatial pattern of FLP expression in the bilateral MVe exhibited the marked difference between the ULX and UNL+ULX groups. MK801 treatment 6 h after ULX showed significant increase in the number of FLP in contralateral MVe (cMVe) of the ULX group, but decrease in cMVe of the UNL+ULX group. These results suggest that the lesion of vestibulocerebellum delays the temporal recovery of FLP expression in MVe and the vestibulocerebellar NMDA receptors relate to FLP expression in MVe.

Effects of inferior olive inactivation and lesion on the activity of medial vestibular neurons in the rat

In anaesthetized rats, the unitary activity from the medial vestibular nucleus had been recorded during horizontal sinusoidal rotation in the absence of visual stimulation. In the first series of experiments, the inferior olivary nuclei were selectively destroyed by means of 3-acetylpyridine. Unitary activity was recorded three to five days or one month after the lesion. A few days after the lesion, the average spontaneous activity, as well as the peak-to-peak amplitude of the modulation of the medial vestibular neurons during sinusoidal rotation, were significantly lower compared to those recorded in intact rats, and to those recorded one month after the lesion. In the second series of experiments, during reversible cooling of the inferior olive region of one side, in the contralateral medial vestibular nuclei 57% of units underwent a clear decrease in firing rate accompanied by a decrease in the amplitude of modulation. In rats whose inferior olivary nuclei had been destroyed by means of 3-acetylpyridine one month before, or whose cerebellum had been removed, there were few units that showed a decrease of the firing rate and modulation amplitude on cooling the same olivary region. Our experiments show that silencing the activity of the inferior olive causes a decrease both in the spontaneous firing rate and in the amplitude of the response of the vestibular neurons to natural labyrinthine stimulation. These results support the hypothesis that the inferior olive, by changing its firing rate, may regulate on-line the gain of reflexes which are under cerebellar control.

Morphology of physiologically identified second-order vestibular neurons in cat, with intracellularly injected HRP.

The morphology of horizontal canal second-order type I neurons was investigated by intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of the cell bodies and axons. Axons penetrated in and around the abducens nucleus were identified as originating from type I neurons by their characteristic firing pattern to horizontal rotation and by their monosynaptic response to stimulation of the ipsilateral vestibular nerve. A total of 47 type I neurons were stained. The cell bodies were located in the rostral portion of the medial vestibular nucleus (MVN) and were large or medium sized and had rather elongated shapes and rich dendritic arborizations. The neurons were divided into two groups: those which projected to the contralateral side of the brain stem (type Ic neurons) and those which projected to the ipsilateral side of the brainstem (type Ii neurons). All stem axons of type Ic neurons crossed the midline and bifurcated into rostral and caudal branches in the contralateral medial longitudinal fasciculus (MLF). Two or three collaterals arising close to this bifurcation distributed terminals in a relatively wide area in the contralateral abducens nucleus. Some of these collaterals projected further to the contralateral MVN and thus are vestibular commissural axons. Some of the rostral and caudal stem axons had collaterals which projected to the contralateral nucleus prepositus hypoglossi (PH), nucleus raphe pontis, or medullary reticular formation. There were at least six classes of type Ii neurons, most of which distributed to a relatively limited region in the ipsilateral abducens nucleus and they were categorized according to their future projections into the following categories: A) no further collaterals beyond the abducens nucleus; B) collaterals in the abducens nucleus and a branch descending and terminating in ipsilateral PH; C) projected to the abducens nucleus, PH, and an area rostral to the abducens nucleus; D) projected to the abducens nucleus and to ipsilateral reticular formation rostral and caudal to the abducens nucleus; E) collaterals in the abducens nucleus and a thick caudal stem axon entering and descending in ipsilateral MLF; F) a thick caudal stem axon entering and descending in ipsilateral MLF and no collaterals to the abducens nucleus. Some type Ii neurons also had recurrent collaterals which projected back to the ipsilateral MVN; these may inhibit type II neurons during ipsilateral rotation.

Neuronal activity in the contralateral medial vestibular nucleus of the guinea pig following unilateral labyrinthectomy

The recovery of normal ocular motor and postural behavior following unilateral labyrinthectomy is termed vestibular compensation and it has been attributed to the return of normal resting activity to neurons in the bilateral vestibular nuclei. Previous studies in the cat have reported that approximately normal resting activity returns to type I neurons in the medial vestibular nucleus (MVN) contralateral to the deafferentiation by 4–8 weeks post-operation (post-op.), while the gain of the response of these neurons to horizontal angular acceleration remains lower than normal. The present data demonstrate that, in the guinea pig, normal resting activity returns to the contralateral MVN type I neurons by only 52–60 h post-op., while the gain and phase of the response of these neurons to horizontal sinusiodal acceleration remains abnormal up to 8–12 months post-op. By contrast with previous studies, the present data show that type II neurons in the contralateral MVN exhibit some increase in their frequency of occurrence and gain toward normal values during vestibular compensation (at 52–60 h and 8–12 months post-op.). The rapid recovery of normal type I resting activity correlates with the disappearance of spontaneous nystagmus and postural asymmetries in the guinea pig by 52 h post-op.

A quantitative [14C]-2-deoxy-D-glucose study of brain stem nuclei during horizontal nystagmus induced by lesioning the lateral crista ampullaris of the rat.

A study of the brainstem of the rat during horizontal nystagmus using the quantitative 2-deoxy-D-glucose technique reflected changes in the functional activity of cell groups based on their glucose utilization rates. Horizontal nystagmus was induced by unilateral crista ampullectomy of the horizontal canal. Comparisons of glucose utilization rates were made between experimental and control groups as well as from side to side within each group. There was a decrease of the ipsilateral medial and superior vestibular nuclei with a concomitant increase in the contralateral medial vestibular nucleus when compared to control. The medial rectus motor division of the ipsilateral oculomotor nucleus showed an increase whereas the ipsilateral abducens and the ipsilateral nucleus prepositus hypoglossi exhibited a decline in their utilization rates. The extra ocular motor nuclei responsible for the excitatory fast phase of nystagmus utilizes more substrate than those involved in the slow phase. An increase was also measured in the ipsilateral lobule of the cerebellar nodulus. The lateral reticular nucleus showed a bilateral decrease in its glucose utilization rate when compared to control.

Commissural and ipsilateral internuclear connection of vestibular nuclear complex of the cat

Commissural and ipsilateral intrinsic connections of the vestibular nuclear complex of cats were investigated using retrograde transport of horseradish peroxidase (HRP). HRP was microiontophoretically injected into limited areas (0.2–0.5 mm in diameter) of the respective vestibular nuclei. In the commissural connections, major fibers were observed between the bilateral superior vestibular nuclei (SVN) and between the bilateral descending vestibular nuclei (DVN); a moderate number of fibers was found from the medial vestibular nucleus (MVN) to the contralateral MVN, SVN and lateral vestibular nucleus (LVN) and from the DVN to the contralateral LVN. Minor commissural connections were detected between the bilateral LVN. The ipsilateral internuclear connections of the vestibular nuclear complex were: (1) from the LVN, MVN and DVN to the SVN, (2) from the MVN and DVN to the LVN and (3) from the MVN to the DVN. Minor ipsilateral intrinsic connections were found from the SVN to the MVN.

Functional organization of premotor neurons in the cat medial vestibular nucleus related to slow and fast phases of nystagmus.

Extracellular spikes were recorded from secondary vestibular neurons in the cat medial vestibular nucleus (MVN) and were identified as type I or II neurons by horizontal rotation. Type I neurons were further classified as excitatory or inhibitory premotor neurons on the basis of their axonal termination in the contralateral or ipsilateral abducens nucleus, demonstrated by spike-triggered averaging of abducens nerve discharges, or by antidromic activation using systematic microstimulation within the abducens nucleus. Both excitatory and inhibitory premotor type I MVN neurons exhibited a rhythmic modulation of their firing rate in association with nystagmus elicited by rotation or electrical stimulation of the vestibular nerve. Their tonic activity during the slow phase was suppressed at the quick phase directed to the ipsilateral side. Excitatory type I MVN neurons terminating in the contralateral abducens nucleus sent collateral axons to the contralateral MVN. These commissural neurons also showed a nystagmus-related discharge pattern. Type II MVN neurons activated at short latency by stimulation of the contralateral vestibular nerve exhibited burst discharges when the activity of ipsilateral type I neurons was suppressed at the quick phase. These type II neurons made monosynaptic inhibitory connection with type I neurons as shown by the post-spike average of the membrane potential of secondary MVN neurons triggered from spikes of single type II neurons. Thus, the inhibitory action originating from burst activity of type II MVN neurons contributes to suppression of type I premotor MVN neurons during fast eye movements.

Ultrastructural study of vestibular and reticular projections to the abducens nucleus.

The origin of the synaptic boutons in the abducens nucleus was studied following lesions of the contralateral medial vestibular nucleus, the ipsilateral paramedian pontine reticular formation and the contralateral dorsomedial part of the reticular formation caudal to the abducens nucleus. Lesions in the rostral part of the contralateral medial vestibular nucleus resulted in degeneration of boutons located mainly on dendritic processes. On the other hand, lesions in both ipsilateral and contralateral reticular formations provoked degenerating terminals on the somata of the abducens neurones and on proximal dendrites in the abducens nucleus beneath of genu of the facial nerve.