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N Hori

Publications and source records attributed to N Hori.

At least 145 records · Page 8Linked to original sources
PubMed1984

N-Methyl-D-aspartate and L-aspartate activate distinct receptors in piriform cortex.

The effects of ionophoretically applied N-methyl-DL-aspartate (NMDA) and aspartate on identified pyramidal neurons in rat piriform cortex were examined in isolated, submerged, and perfused brain slices. NMDA was more potent than aspartate in eliciting neuronal discharge. Perfusion of the acidic amino acid antagonists, DL-2-amino-5-phosphonovalerate (APV), 10(-6) or 10(-5) M, DL-2-amino-7-phosphonoheptanoate (APH), 10(-5) M, and gamma-D-glutamylglycine (gamma DGG), 10(-5) M, selectively blocked the response to NMDA without effect on the response to aspartate. At higher concentrations which blocked responses to both NMDA and aspartate, gamma DGG blocked kainate responses and depressed glutamate and quisqualate responses. These results suggest that in piriform neurons NMDA and aspartate act at distinct receptor sites, not a common receptor site, and that both of these sites are distinct from those that mediate responses to glutamate, quisqualate, and kainate.

2-Amino-5-phosphonovalerate↗
PubMed1984

[Amikacin concentration in the severely obstructed urinary tract].

Urinary amikacin concentration was determined in 9 patients with severely unilateral ureteral obstruction. Serum levels were within the normal range. The average concentration of amikacin in the urine from obstructed urinary tract was 118.9 mcg/ml 6 hours after 100 mg amikacin iv infusion. Urine concentration from the normal kidney was 155.9 mcg/ml at the first 2 hours after intravenous infusion, 98.8 at the second 2 hours 83.3 at the third 2 hours. Urinary amikacin excretion from severely obstructed urinary tract was about one third of the total excretion from a normal system. In summary, the urinary level in severely obstructed urinary tract after iv infusion of 100 mg amikacin may be enough prophylactically. But at the onset of infection in severely obstructed urinary tract, the administration of at least 200 mg amikacin intravenously is required.

Adult↗
PubMed1983

Asymmetric distribution of acetylcholine receptors and M channels on prepyriform neurons.

The responses of pyramidal neurons of rat prepyriform cortex to ionophoretic application of acetylcholine (ACh) were studied in a submerged, perfused brain slice. ACh excited some neurons but only if applied to an area near to the cut surface of the slice. This area contained the basal dendrites of the pyramidal cells and some cell bodies. No excitation was seen if ACh was applied at depths of 250 microns or more from the cut surface, an area which contained only apical dendrites, although the apical dendrites were very sensitive to excitatory amino acids such as aspartate (Asp) and glutamate (Glu). On all neurons which did not discharge to ionophoretic application of ACh, ACh potentiated the response to Glu and Asp. No potentiation of amino acid responses was obtained on apical dendrites. The potentiation had a time course similar to that of the discharge of neurons which fired to ACh. This observation suggests that pyramidal neurons have receptors for ACh on basal but not apical dendrites. The ACh response in the basal dendrite-soma region was elicted by pilocarpine and blocked by atropine but not curare. This was true whether the response studied was direct excitation or potentiation of the response to an amino acid. The ACh response was associated with a voltage-dependent increase in membrane resistance which had a slow time course and appeared to be due to a turning off of an M current, as described by Brown and Adams (1980) in sympathetic ganglion cells. The effects of ACh were minimal at the resting potential but increased with depolartization. ACh had no effect on the current-voltage relation of the cell, except at depolarized potentials of less than -60 mV. Ionophoretic application of Ba2+ to the basal dendritic region resulted in potentiation of the amino acid responses and sometimes induced a discharge similar to that of ACh. Since Ba2+ mimics the ACh response, presumably by a direct blockade of the M channel, the effects of Ba2+ on apical dendrites were tested to determine whether these dendrites contain M channels associated with a transmitter receptor other than ACh. However, Ba2+ did not induce potentiation in apical dendrites, suggesting that M channels are also restricted to the basal dendrites or cell bodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1983

[Effect of suloctidil on the reduced evoked potentials in brain slices in low glucose perfusate].

Effects of suloctidil [erythro-1-(4-isopropylthiophenyl)-2-n-octylaminopropanol] on reduced evoked potentials in low glucose perfusate were studied using guinea-pig prepyriform cortex in vitro. The amplitude of evoked potential to paired electrical stimulation of the olfactory tract in cerebral slices was consistently and reversibly suppressed by the perfusion with low glucose (3 mM)-Krebs-Ringer's solution. The amplitude reduction after 10 min exposure to the perfusate was fairly reproducible in the same preparation. The amplitude reduction was always accompanied with significant facilitation of "postactivation potentiation", estimated from the size of the first and second response to paired stimulation. Perfusion of brain slices with low glucose Krebs-Ringer's solution containing 10(-7)-10(-6) g/ml suloctidil for 10 min, however, effectively prevented the reduction of amplitude of evoked potentials to below 30-50% of the control value. The facilitation of postactivation potentiation under the low glucose condition was also suppressed by the drug. Dihydroergotoxin, 3 X 10(-6) g/ml, also showed a comparable effect as 10(-6) g/ml suloctidil. These data suggest that suloctidil possesses a brain energy economizing effect such as activation of oxygen, glucose uptake or production of high energy substance.

Animals↗
PubMed1983

[A clinical survey on 24 cases of primary ureteral tumors].

A clinical survey was performed on 24 cases of primary ureteral tumors treated in our University Hospital between Jan. 1972 and Dec. 1981. The incidence of primary ureteral tumors was 0.17% among the outpatients in our urologic clinic. The patients ranged from 41 to 84 years old in age (average age: 65 years), and the male to female ratio was 3 to 1. The left ureter and the lower third of the ureter were involved more frequently. The most frequent initial symptom was macrohematuria seen in 19 cases (79%), followed by loin pain seen in 6 cases (25%). A cytologic study of the voided urine or ureteral urine was carried out in 18 cases and positive results were obtained in 9 cases (50%). Cystoscopic examination revealed a tumor protruding through the ureteral orifice in 16.7% (4 of 24 cases), followed by bulging orifice in 8.3% (2 of 24 cases). Excretory pyelography showed ureteral filling defects in 41.7% (10 of 24 cases). Retrograde pyelography showed ureteral filling defects in 100% (10 of 10 cases). CT showed a mass region in 44.4% (4 of 9 cases). A total of 14 patients underwent nephroureterectomy with partial or total cystectomy (66.7%). The overall 5-year-survival rate was 56.5% and could be directly associated with grade and stage of tumors.

Adult↗
PubMed1982

Neuronal control of the ventromedial nucleus from the periventricular nucleus in the hypothalamic slice of the rat.

A neuronal pathway between periventricular nucleus and ventromedial hypothalamus (VMH) was investigated by both anatomical and electrophysiological methods. Horseradish peroxidase (HRP)-labelled clusters were observed in the periventricular nucleus after application of HRP into the VMH. Periventricular nucleus stimulation produced mainly excitation of VMH neurones with a latency of 3 msec. These results suggest that periventricular nucleus sends information in the cerebro-spinal fluid to the VMH.

Animals↗
PubMed1982

Pharmacologic sensitivity of amino acid responses and synaptic activation of in vitro prepyriform neurons.

1. In an effort to identify the neurotransmitter released from terminals of the lateral olfactory tract (LOT) we have studied excitatory amino acid agonist and antagonist actions on population and single-unit responses in submerged and perfused slices of rat prepyriform cortex. Previous studies suggest that the transmitter at this synapse is either aspartate (Asp) or glutamate (Glu). 2. The field potential reflecting the monosynaptic activation of pyramidal neurons after stimulation of the LOT was reversibly depressed by bath perfusion of agonists, with an order of potency being kainic acid (KA) greater than N-methyl-DL-aspartate (NMDA) greater than homocysteic acid (HC) greater than Asp = Glu. 3. The synaptic field potential was essentially unaffected by DL-alpha-aminoadipic acid (AA), 2-amino-3-phosphonopropionic acid (APP), and DL-alpha-diaminopimelic acid (DAPA), all presumed to be selective for Asp receptors, and by L-glutamic acid diethyl ester (GDEE), presumed to be specific for Glu receptors. The field potential was depressed or abolished by 2-amino-4-phosphonobutyric acid (APB), an agent known to block Glu responses in insect muscle. 4. The effects of ionophoretic application of agonists were studied on single neurons recorded extracellularly. While there was some variability among neurons in relative agonist potency, all neurons were excited by the five agonists with relative potencies in general similar to those observed for the field potentials. 5. Responses to Glu and Asp were unaffected by AA, GDEE, and APB at concentrations up to 5 X 10(-3) M. Responses to KA, NMDA, and HC were often depressed by APB but were unaffected by the other antagonists. The excitation on stimulation of the LOT was consistently, rapidly, and reversibly blocked by APB. 6. These observations are not consistent with either Glu or Asp being the neurotransmitter of the LOT.

Animals↗
PubMed1981

Lateral olfactory tract transmitter: glutamate, aspartate, or neither?

Aspartate and glutamate are the principal candidates for the excitatory neurotransmitter released by the lateral olfactory tract (LOT) in prepyriform cortex of the rat. Identity of action of the natural transmitter with exogenous glutamate and/or aspartate, however, has not yet been demonstrated. We show that bath-applied 2-amino-4-phosphonobutyric acid, a presumed specific glutamate antagonist, blocks LOT-stimulated prepyriform field potentials and single unit activity but not the single unit response to ionophoretically applied glutamate or aspartate in rat olfactory cortex slices. These results suggest that neither aspartate nor glutamate is the LOT transmitter. Responses to ionophoretically applied N-methyl-DL-aspartate, kainic acid, and DL-homocysteate were clearly decreased by 2-amino-4-phosphonobutyric acid. This suggests that these agents, usually presumed to be aspartate or glutamate agonists, act at different receptors than aspartate and glutamate.

Aminobutyrates↗
PubMed1981

A new method for application of horseradish peroxidase into a restricted area of the brain.

A new method for horseradish peroxidase (HRP) application into the very restricted area of the brain was developed. Crystalline HRP was packed into the tips of fine micropipettes having tip size of about 50 micrometer in outer diameter. The HRP micropipettes were stereotaxically implanted into the globus pallidus of rats. After survival period of 6 to 48 hours, brain was excised and HRP distribution was investigated following conventional procedures. The diffusion area of HRP at the application site was restricted within the limits of 200--250 micrometer in diameter completely inside the globus pallidus. It was known that the slowly solubilized crystalline HRP was taken up by the nerve terminals in the globus pallidus, and transported retrogradely to the cell bodies in the pars compacta of substantia nigra, indicating the existence of nigro-pallidal projections.

Animals↗
PubMed1980

Effect of calcium removal on thermosensitivity of preoptic neurons in hypothalamic slices.

Extracellular single-unit activities of thermosensitive neurons were recorded from the medial preoptic area in rat's hypothalamic slices in vitro. Of 256 preoptic units, 74 were warm-units which increased firing rates in response to a rise in slice temperature and 16 units were cold-units having the opposite type of thermosensitivity. Eighteen of 23 warm-units and 3 of 4 cold-units retained their thermosensitivities during perfusion with Ca2+-free/high Mg2+ salt solution. The thermosensitivities of the remaining 5 warm-units were reversibly abolished in the Ca2+ deficient medium. The results suggest that some warm- and cold-sensitive neurons in the medial preoptic area have an inherent thermosensitivity.

Animals↗
PubMed1980

[Protective effect of suloctidil against cerebral hypoxia (author's transl)].

The protective effect of suloctidil [MY 103, erythro-1-(4-isopropylthiophenyl)-2-n-octylaminopropanol] against cerebral hypoxia was investigated in terms of survival time under normobaric hypoxia (96% N2 + 4% O2 gas mixture) in mice and evoked potential in prepyriform cortex of guinea pig in vitro. In a hypoxic condition, the pretreatment with MY 103 (3.0-12.5 mg/kg, i.p.) resulted in a marked and dose-dependent prolongation of survival time of mice without any adverse effect. The prolongation of survival time was statistically significant at doses over 6.3 mg/kg. The amplitude of evoked potential to electrical stimulation of olfactory tract in the brain slice was consistently and reversibly suppressed by the perfusion with low oxygen Ringer's solution containing about 45% O2 or normal Ringer's solution. This amplitude reduction after 6 minutes exposure to hypoxic perfusate, was consistently reproducible in the same preparation. Preincubation of brain slices in normal Ringer's solution containing 10(-7)-10(-6) g/ml MY 103 for 15 min, however, effectively prevented the hypoxic reduction of the amplitude of evoked potentials to 30-50% of the control experiments. The above data indicate that MY 103 exerts its anti-anoxic effect presumably through modified metabolic processes such as active oxygen or glucose uptake by the brain.

Animals↗