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Biomedical subjects

N Furuya

Publications and source records attributed to N Furuya.

At least 127 records · Page 7Linked to original sources
PubMed1986

Synaptic connections of horizontal canal mediated ascending Deiters tract axons on medial rectus motoneurons in cat.

This study demonstrates the termination of ascending tract of Deiters' (ATD) axons on ipsilateral medial rectus (MR) motoneurons. Horseradish peroxidase (HRP) was iontophoretically injected into ATD axons which were recorded in the MR motoneuron pool of the oculomotor nucleus. MR motoneuron cell bodies were identified by retrograde transport of HRP injected into MR muscles in the orbit. ATD axons were identified by Type I responses to horizontal rotation, monosynaptic responses on stimulation of the ipsilateral labyrinth, and no response on contralateral labyrinth or contralateral abducens nucleus or on ipsilateral MR nerve stimulation. Light microscopic examination showed the main stem axons to be lateral to the medial longitudinal fasciculus, and terminal boutons were in contact with ipsilateral identified MR motoneurons (Furuya and Markham: Exp. Brain Res. 43: 289-303, 1981). Light microscopy and semi-thin sections showed boutons of ATD in contact with identified MR motoneuron cell bodies and proximal dendrites. The electron micrographs (EM) showed the HRP-injected ATD axons have synapses on MR motoneurons. ATD boutons made axosomatic and axodendritic synapses on MR motoneurons. The boutons contained numerous spheroidal synaptic vesicles. Several examples showed clear asymmetrical post-synaptic membrane specialization. This confirms the synaptic connection between horizontal canal activated elements in the ATD and MR motoneurons.

Abducens Nerve↗
PubMed1986

Predominance of nasal over temporal saccades in fast eye movement.

Quantitative analysis of saccadic eye movement caused by 20 degree amplitude gaze in horizontal plane was undertaken in 131 subjects using the Contraves' computerized oculomotor testing system. All of the subjects were free from any spontaneous nystagmus, neurological symptoms, and abnormalities of vestibular function. Both of the monocular recordings of saccade were made with a 3 sec time constant, 25 Hz high-cut filter, and digitized with a 3.9 msec sampling time. Four parameters i.e., maximum velocity, gain, latency, and duration, were analyzed. The average (S.D.) of each parameter was 337.1 (65.7) degree/sec, 1.00 (0.14), 199.1 (44.0) msec, and 128.3 (20.2) msec, respectively. We discussed the differences between nasal saccade and temporal saccade. The former was faster than the latter in maximum velocity and shorter in duration, while no differences were recognized in latency. It is suggested that the predominance of nasal saccade in fast eye movement is due to the anatomical difference of the vestibulo-ocular pathway between the medial rectus and the lateral rectus. In other words, because the synaptic inputs to the medial rectus are excitatory as opposed to the inhibitory and excitatory the inputs to the lateral rectus, the difference in muscle tone between the two muscles results in a faster maximum velocity of nasal saccades in fast eye movement.

Adult↗
PubMed1984

Direct projection of pause neurons to nystagmus-related excitatory burst neurons in the cat pontine reticular formation.

Brain-stem pause neurons (PNs) are inhibitory neurons which cease their tonic firing about 20 ms prior to the quick phase of horizontal vestibular nystagmus in either direction. One group of nystagmus-related burst neurons just rostral to the abducens nucleus exhibits a burst of spikes before and during the quick phase to the ipsilateral side--excitatory burst neurons (EBNs). The present study supported the conclusion that PNs project to, and tonically inhibit EBNs during the slow phase and that the burst of activity of EBNs at the quick phase is partly caused by the abrupt release from pauser inhibition. The evidence leading to this conclusion is: simultaneous recording of PNs and EBNs showed close alternation of firing; PNs were antidromically activated from the EBN region; systematic microstimulation tracks within the EBN region showed an antidromic activation pattern of low threshold sites separated by high threshold sites consistent with PN axonal branching in the EBN region; during the nystagmus slow phase there were positive field potentials in the EBN region, followed by an abrupt negative deflection whose onset was synchronous with the last pauser spike; when single PN spikes were used to trigger averages of extracellular field potentials in the EBN region (postspike averaging), a consistent short-latency positivity was observed. This study shows an additional connection in the premotor neural network responsible for the generation of the quick phase of horizontal vestibular nystagmus.

Action Potentials↗
PubMed1981

Arborization of axons in oculomotor nucleus identified by vestibular stimulation and intra-axonal injection of horseradish peroxidase.

Axons in the medial rectus (MR) subdivisions of the oculomotor nucleus were identified by horizontal rotation and by electrical stimulation of the vestibular nerves and abducens nuclei. Three types of axons (vestibular type I and II and abducens interneurons) were then injected intra-axonally with horseradish peroxidase (HRP). Each injected axon was reconstructed under the microscope in the frontal and horizontal planes and terminal arborization and boutons contacting with MR motoneurons were studied. The MR motoneurons were identified by retrograde uptake of HRP, HRP being injected in the MR muscle prior to the intra-axonal experiment. The main types of horizontal canal-related axons were as follows: (1) ATD-unilateral termination axons: Most type I axons were of this type. Axons ascended in ascending tract of Deiters (ATD) to the oculomotor nucleus and terminated in ipsilateral MR area. (2) ATD-bilateral termination axons: Very few secondary canal responsive axons were in this group. Axon ascended in ATD to the oculomotor nucleus and terminated in MR motoneuron areas bilaterally and in Edinger-Westphal nucleus. (3) MLF-bilateral termination axons: Most type II neurons were in this group. Axons went up in the contralateral MLF and into both oculomotor nuclei. Their branches distributed to several motoneuron areas but only infrequently to the MR area; and to the Edinger-Westphal nucleus. (4) AB interneuron axons: Axons ascended in the MLF contralateral to cells of origin and terminated in the contralateral MR motoneuron area.

Abducens Nerve↗
PubMed1976

Transcerebellar inhibitory interaction between the bilateral vestibular nuclei and its modulation by cerebellocortical activity.

In decerebrate, unanesthetized cats, the brain stem was longitudinally cut at the midline from its dorsal to ventral surface with the cerebellum kept intact, eliminating neural interactions between the bilateral vestibular nuclei through the brain stem. Extracellular spike potentials of vestibular type I neurons identified by horizontal rotation were distinctly inhibited by contralateral vestibular nerve stimulation. This crossed inhibition was abolished by removal of the medial part of the cerebellum, indicating that the inhibition was mediated through the cerebellum. Neither aspiration of the flocculus on the recording side nor intravenous administration of picrotoxin eliminated transcerebellar crossed inhibition, suggesting that it is mediated through the cerebellar nuclei. When the fastigial, interposite and dentate nuclei were stimulated, inhibition of vestibular type I neurons was produced only from the contralateral fastigal nucleus. Cerebellocortical stimulation which inhibited fastigial type I neurons suppressed transcerebellar crossed inhibition. Effective sites for suppression of transcerebellar crossed inhibition were localized to lobules VI and VIIa in the vermal cortex on the side of labyrinthine stimulation. Intracellular recordings were made from type I neurons in the medial vestibular nucleus. Stimulation of the contralateral vestibular nerve and the contralateral fastigial nucleus produced IPSPs in these neurons with the shortest latency of 3.8 msec and 1.8 msec, respectively. The difference between these two latency values approximates the shortest latency of spike initiation of fastigial type I neurons in response to vestibular nerve stimulation. It is postulated that transcerebellar crossed inhibition is mediated through the fastigial nucleus on the side of labyrinthine stimulation.

Brain Stem↗
PubMed1976

A substrain mouse serologically classified in ddN strain and its behavioral characteristics.

A special substrain mouse in ddN strain was classified by cross agglutination reaction of the red blood cells with anti-ddN mice red blood cells rabbit immune serume. The agglutination reactivity in the full-grown substrain mouse was as high as in an infant ddN mouse. Incidence of the substrain mouse in ddN strain aged older than 9 weeks was about 10%. The full-grown substrain mouse revealed a form of excitation after long-term administration of methamphetamine while other mice in the same strain were depressed. The behavioral and serological properties of histocompatible strain mice such as C57Bl and C3/ were studied to compare with those of the ddN substrain mouse.

Age Factors↗
PubMed1975

Functional organization of vestibulofastigial projection in the horizontal semicircular canal system in the cat.

Spike potentials of fastigial nucleus neurons were recorded extracellularly in decerebrate, unanesthetized cats. The neurons responding to head rotation in the horizontal plane with a type I fashion were located mainly in the middle and caudal regions of the fastigial nucleus. Three fourth of these fastigial type I neurons were antidromically activated by stimulation of the contralateral vestibular nuclei. These neurons were excited transsynaptically from the ipsilateral vestibular nerve or nuclei. Intra cellular recordings were made from those neurons which were located in the caudal half of the fastigial nucleus and were activated antidromically from the contralateral vestibular nuclei. Stimulation of the ipsilateral vestibular nerve produced EPSPs in these neurons with latencies of 1.0-6.6 msec. The shortest conduction time along primary vestibular aggerents from the labyrinth to the ipsilateral fastigial nucleus was 0,7 msec. The EPSPs with the shortest latency of 1.0 msec were therefore postulated to be due to monosynaptic connections of primary vestibular afferents with fastigial neurons. Stimulation of ipsilateral vestibular nuclei also produced monosynaptic EPSPs in fastigial neurons. These EPSPs were facilitated by conditioning stimulation of the ipsilateral vestibular nerve, indicating the existence of polysynaptic activation of fastigial neurons from the ipsilateral vestibular nerve through the vestibular nuclei.

Animals↗