Disease relevance of Vestibular Nuclei

• Either complete OTR or skew torsion without head tilt indicates a unilateral peripheral deficit of otolith input or a unilateral lesion of graviceptive brainstem pathways from the vestibular nuclei (crossing midline at the pontine level) to the interstitial nucleus of Cajal (INC) in the rostral midbrain [1].
• Immunohistochemical detection of phosphorylated form of extracellular signal-regulated kinase 1/2 in rat vestibular nuclei following hemorrhagic hypotension [2].
• By contrast, infarctions in the vestibular nuclei only appeared at the higher SRIF dose [3].
• The results indicate that scopolamine and dimenhydrinate exert their effect in motion sickness by reducing the vestibular and visual influx and by partly inhibiting the integrative functioning of the vestibular nuclei [4].
• To elucidate the effectiveness of the drug in the treatment of vertebrobasilar insufficiency (VBI), we performed an electrophysiological study to examine the effects of ipenoxazone hydrochloride, a glutamate blocker, on hypoxia-induced firing in the medial vestibular nucleus (MVN) neuron, using alpha-chloralose-anesthetized cats [5].

High impact information on Vestibular Nuclei

• Synaptic plasticity in the medial vestibular nuclei: role of glutamate receptors and retrograde messengers in rat brainstem slices [6].
• This resulted in a complete lack of Fos labeling in the vestibular nuclei and the inferior olive, and a significant reduction in labeling in other nuclei in the off-axis condition, indicating that these nuclei have a significant labyrinth-sensitive component to their Fos labeling [7].
• The effects of thiamine (B1) deficiency on local CMRglu (LMCRglu) in the vestibular nuclei were studied with the 14C-2-deoxyglucose autoradiographic method in awake asymptomatic and symptomatic rats [8].
• In parallel with the modifications in synaptic plasticity, we observed that the expression patterns and localizations of mGluR5 and mGluR1 in the medial vestibular nuclei (MVN) changed during postnatal development [9].
• The changes in GABA receptor efficacy after UL are therefore not due to the vestibular de-afferentation itself, but are instead due to the imbalance in excitability of the vestibular nuclei of the lesioned and intact sides, and the enhanced commissural inhibition of the ipsi-lesional MVN cells that follows UL [10].

Biological context of Vestibular Nuclei

• Developmental shift from long-term depression to long-term potentiation in the rat medial vestibular nuclei: role of group I metabotropic glutamate receptors [9].
• Fast inhibitory synaptic transmission in the medial vestibular nucleus (MVN) is mediated by GABA(A) receptors (GABA(A)Rs) and glycine receptors (GlyRs) [11].
• Neuronal plasticity reorganizations in the vestibular nuclei following unilateral labyrinthectomy appear to include only changes in NR1 and NR2C mRNA levels modifying the functional diversity of the NMDA receptor in the ipsilateral medial vestibular nucleus neurons [12].
• 5.) From the experiments it can be concluded that the inhibitory transmitter GABA plays an important role for eye movement generation within the vestibular nuclei [13].
• The highest numbers of glutamate binding sites were observed in the medial vestibular nuclei [14].

Anatomical context of Vestibular Nuclei

• The NR2C immunoreactivity emerged 5 days after birth in the olfactory bulb, thalamus, and vestibular nuclei and became very intense after 10 days in cerebellar granule cells, its primary site of expression in adulthood [15].
• 1. We examined the synaptic activation of N-methyl-D-aspartate (NMDA) receptors by stimulation of primary vestibular afferent projections to second-order neurons in the medial vestibular nucleus (MVN) using whole cell patch-clamp recording methods in rat brain stem slices maintained in vitro [16].
• MK801 also induced Fos expression in fastigial and vestibular nuclei, but not in lateral (interpositus and dentate) cerebellar nuclei [17].
• After lesion of the vestibular nerve, no calretinin staining was seen in any of the vestibular nuclei except for a population of intrinsic neurons, which showed no obvious change in number or staining pattern [18].
• The present study describes the complete course and terminations of Calb+ PVA in the cerebellar cortex, the cerebellar (CN) and vestibular nuclei (VN) of the mouse [19].

Associations of Vestibular Nuclei with chemical compounds

• Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat [20].
• The synaptic activation of N-methyl-D-aspartate receptors in the rat medial vestibular nucleus [16].
• Microiontophoresis of acetylcholine, histamine and their antagonists on neurones in the medial and lateral vestibular nuclei of the cat [21].
• Previous anatomic and electrophysiological evidence suggests that serotonin modulates processing in the vestibular nuclei [22].
• An influence of noradrenergic systems on the vestibular function by a direct action of noradrenaline inside the vestibular nuclei is proposed [23].

Gene context of Vestibular Nuclei

• In vestibular nuclei, the NR1 subunit mRNA was found in various populations of neurons [12].
• Calretinin levels in the vestibular nuclei, increased significantly between birth and postnatal day (P) 45 [24].
• We investigated whether three calcium-binding proteins, calretinin, parvalbumin, and calbindin, could identify specific aspects of the postnatal development of the rat lateral (LVN) and medial (MVN) vestibular nuclei and their vestibular and cerebellar connections [24].
• In the VN, Calb+ PVA terminations were restricted to the superior, the ventral part of the lateral, the lateral portion of the medial, and the inferior vestibular nuclei [19].
• 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) [25].

Analytical, diagnostic and therapeutic context of Vestibular Nuclei

• 4. The splanchnic nerve responses to head rotation could be abolished by microinjections of the excitotoxin kainic acid into the medial and inferior vestibular nuclei, which is concordant with the responses resulting from activation of vestibular receptors [26].
• The localization of neurons expressing mRNAs for the NR1 and NR2A-D subunits of the glutamatergic NMDA receptor was examined by non-radioactive in situ hybridization throughout the guinea pig vestibular nuclei [12].
• Following unilateral inner ear lesion in rats, the medial vestibular nuclei were probed with Na alpha I, Na alpha III, SK1, SK2 and SK3 oligonucleotide probes: autoradiography indicated no difference between the two sides, at any of the times studied [27].
• To explore this possibility, the effects of electrical stimulation of the medial vestibular nucleus (MVN) on the firing rates of hippocampal CA1 neurons in the urethane-anesthetized rat were investigated using extracellular single unit recordings [28].
• The function of the 5-hydroxytryptamine (5-HT) system in the medial vestibular nucleus (MVN) was evaluated using KCl-evoked 5-HT release assessed by in vivo microdialysis [29].

References