Izuru Matsuoka

Locus coeruleus-induced inhibition of dorsal cochlear nucleus neurons in comparison with lateral vestibular nucleus neurons.

The effects of conditioning stimulation of the locus coeruleus (LC) on the neuron activity of dorsal cochlear nucleus (DCN), which is rich in noradrenergic nerve terminals, were compared with those on the lateral vestibular nucleus (LVN), devoid of such terminals, to determine whether or not noradrenaline is responsible for the LC-induced inhibition. The conditioning stimuli applied to the LC had no effect on either the field potential or the spike generation of mono- and polysynaptic neurons in the LVN elicited by VIIIth cranial nerve stimulation. In contrast, the spike firing of the DCN neurons with VIIIth cranial nerve stimulation was significantly inhibited by LC conditioning stimulation. The inhibition of spike generation was mainly observed in the DCN neurons which fired spikes with a longer latency. The inhibition of DCN neurons by LC conditioning stimulation did not occur in the cats pretreated with reserpine; however, a rapid recovery of the inhibition was produced by intraventricular application of noradrenaline. These results are in good agreement with the histochemical findings and support our previous conclusion that noradrenaline acts as an inhibitory transmitter or modulator on the nuclei where noradrenergic nerve terminals derived from the LC are located. In addition, the vestibular input in the primary relay nucleus is apparently not regulated by noradrenaline originating in the LC.

Afferent projection from reticular nuclei, inferior olive and cerebellum to lateral vestibular nucleus of the cat as demonstrated by horseradish peroxidase

Afferent connection to lateral vestibular nucleus (LVN) was examined using retrograde transport of horseradish peroxidase (HRP). When HRP was microiontophoretically applied to the immediate vicinity of the LVN neuron, which monosynaptically fired spike upon VIIIth cranial nerve stimulation, HRP-labelled cells were observed in the ipsilateral lateral reticular nucleus, bilateral gigantocellular nucleus, and contralateral dorsal cap and beta-nucleus of inferior olive in addition to various parts of cerebellum.

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.

Equilibrium disorders with diffuse brain atrophy in long-term toluene sniffing

SummaryA Japanese male who became habituated to sniffing toluene exhibited ataxia, tremor, incoordination and equilibrium disorders. There was pendular nystagmus with a normal caloric response. There were an inhibition of optokinetic nystagmus and a failure to follow over 0.1 Hz sine waves on eye tracking test. Angiogram and pneumoencephalogram revealed an atrophy of the midbrain and cerebrum, and degeneration of the cerebellum was suspected.

Transdermally administered scopolamine vs. dimenhydrinate. II. Effect on different types of nystagmus.

The effects of transdermally administered scopolamine (TTS-scopolamine) (release rate 5 micrograms/h, one and two patches) and dimenhydrinate (100 mg) on caloric, angular acceleration induced and optokinetic nystagmus were examined in 16 volunteers in a randomized double-blind study. All drugs induced a statistically significant decrease in maximum velocity of caloric nystagmus, as compared with placebo. In the rotatory test, two TTS-scopolamine and dimenhydrinate reduced the vestibular gain significantly. No changes were observed in time constant. In the optokinetic test, all drugs tended to reduce the responses, but a statistically significant reduction was found only after two TTS-scopolamine. The results indicate that the drugs effective against motion sickness reduce the nystagmic response, which at least partly explains the mode of action of the drugs. The target organ of the drugs is presumably the vestibular nucleus, where vestibular and visual impulses are integrated to ensure optimal gain for vestibular orientation reflexes.

Experimental vestibular pharmacology: a minireview with special reference to neuroactive substances and antivertigo drugs.

Neurotransmitters and neuromodulators involved in the function of vestibular nuclei were reviewed with special reference to drugs used for treatment of motion sickness and vertigo. Biochemical, histochemical and electrophysiological studies have demonstrated that acetylcholine is a transmitter candidate from the afferent vestibular nerve to the lateral vestibular nucleus (LVN), because acetylcholine satisfies most criteria for a chemical transmitter in the central nervous system. It is unlikely, however, that monoamines such as noradrenaline, dopamine and serotonin are transmitters in the vestibular neurons, since cell bodies and nerve terminals containing the monoamines have not been detected yet in the vestibular nuclei. Although histamine and H1-receptor blockers inhibit neuron activities in the vestibular nuclei, it is unclear at present whether histaminergic system is directly related to the function of vestibular neurons. It has been established that GABA is an inhibitory transmitter from the cerebellar Purkinje cells to the LVN neurons. Diazepam is considered to enhance the GABA effect on the LVN, thereby modifying the vestibular neuronal firing. Enkephalin-containing cell bodies and nerve terminals are found in the medial vestibular nucleus, and a few substance P-containing neurons have been observed in the vestibular nuclei. However, the functional role of these peptides on the vestibular system remains to be determined. Unlike histamine H1-receptor blockers, vasodilators such as cinnarizine, ifenprodil and adenosine triphosphate, which are effective in treatment of vertigo, produce an enhancement of responsiveness of neuron activities in the vestibular nuclei, probably as a result of an increase in blood flow in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic Evidence for Involvement of Acetylcholine as a Neurotransmitter in the Lateral Vestibular Nucleus

Monosynaptic spike generation of lateral vestibular nucleus (LVN) neurons with vestibular nerve stimulation in cats was inhibited by microiontophoretic atropine and gamma-aminobutyric acid (GABA). Spontaneous firing of the LVN monosynaptic neuron was increased by iontophoretic acetylcholine and glutamate. Atropine inhibited acetylcholine-induced firing without affecting glutamate-induced firing, while GABA blocked spike generation produced by acetylcholine and glutamate. Acetylcholine probably plays a role in transmission from the vestibular nerve to the LVN monosynaptic neurons.

Inhibitory effect of betahistine on polysynaptic neurons in the lateral vestibular nucleus

ZusammenfassungDie Untersuchung der Wirkung von Betahistin, einem Medikament zur Beeinflussung des Schwindels, auf den Nucleus vestibularis lateralis der Katze, zeigte eine Erregungshemmung der polysynaptischen Neurone, während die Reaktion der monosynaptischen unbeeinflußt blieb.SummaryEffects of betahistine, an antivertigo drug, were examined on the lateral vestibular nucleus (LVN) neurons of cats anesthetized with α-chloralose. Spike generation of monosynaptic LVN neurons elicited by vestibular nerve stimulation remained unaffected with intravenous administration of betahistine up to 5 mg/kg and with iontophoretic application of the drug up to 200 nA. In contrast, the spike generation of polysynaptic I neurons in the LVN was dose-dependently inhibited by intravenous as well as iontophoretic application of betahistine. These results suggest that small doses of betahistine more selectively interfere with synaptic transmission in the polysynaptic I neurons than in the monosynaptic neurons.

Vestibular efferent fibers to ampulla of anterior, lateral and posterior semicircular canals in cats

Origins of vestibular efferent fibers to ampulla of semicircular canals in cats were examined using retrograde transport of horseradish peroxidase. The anterior canal was innervated from bilateral parvocellular reticular nucleus (PCRN), contralateral gigantocellular reticular nucleus and ipsilateral lateral reticular nucleus (LRN); the lateral canal, from ipsilateral PCRN and LRN as well as ipsilateral lateral vestibular nucleus; and the posterior canal, from bilateral PCRN and ipsilateral medial and lateral vestibular nuclei.

Effects Of Cholinergic Agonists And Antagonists On Nucleus Vestibularis Lateralis Unit Discharge To Vestibular Nerve Stimulation In The Cat

Unit discharge in nucleus vestibularis (NVL) was studied in locally anesthetized cats. The mean firing rate +/-S.E. of spontaneous unitary discharges of NVL neurons was 19.8+/-0.9 Hz and that of spinal-transected animals was 18.0+/-1.6 Hz. The mean firing rate of these neurons in animals with cerebellum ablation and the administration of scopolamine in a dose of 0.5 mg/kg i.v. was relatively low. After administration of physostigmine in a dose of 25 mug/kg i.v. the firing rate was enhanced. The effects of physostigmine were antagonized by scopolamine. About 95% of NVL neurons activated by single electrical shocks to the ipsilateral vestibular nerve showed regular firing following administration of physostigmine. These neurons changed to a gamma distribution at lambda=2 following administration of scopolamine.