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Volume 97 (1991)
- Issue 6 Pages 307-
- Issue 5 Pages 241-
- Issue 4 Pages 179-
- Issue 3 Pages 135-
- Issue 2 Pages 51-
- Issue 1 Pages 1-
Volume 97, Issue 4
Displaying 1-6 of 6 articles from this issue
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Nobukuni OGATA, Hideharu TATEBAYASHI1991 Volume 97 Issue 4 Pages 179-189
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSBaclofen, a β-chlorophenyl derivative of γ-aminobutyric acid (GABA), depresses neuronal excitability in various parts of the central nervous system. The site of action for this drug had once been considered to be distinct from GABA recognition sites. In addition to the classical GABA recognition site (GABAA site), a new class of GABA receptor (GABAB site) has been characterized. GABAB sites are mainly present on nerve terminals and, when activated, result in diminished transmitter release, probably through a reduction in Ca2+ influx. Baclofen was shown to be a selective agonist for this novel GABAB recognition. Baclofen also directly hyperpolarizes the membrane of mammalian brain neurons, in addition to its pretynaptic action. This postsynaptic action of baclofen was shown to result from an increase in K+ conductance when studied in hippocampal pyramidal neurons through postsynaptic GABAB receptors. Thus, the inhibitory neurotransmitter GABA activates two receptor subtypes that can be distinguished by their physiological and pharmacological properties. GABAA receptors mediate rapid alterations in the distribution of Cl- across the membrane. GABAA receptors are linked directly to an ion channel, thus contributing to the prompt inhibition of cellular excitability. On the contrary, the GABAB receptor does not contain an integral ion channel and is thus responsible for slower responses through receptor-G-protein-effector complexes. G-protein may be directly coupled to K+ or Ca2+ channels. In addition, G-protein may modulate a variety of regulatory proteins or second messengers, thus contributing to the slower alteration of cellular excitability or to the modulation of neurotransmitter release.View full abstractDownload PDF (8375K) -
Mihoko TANAKA, Katsuhiko NAKATA, Kenji TAKASE, Shiro MITA1991 Volume 97 Issue 4 Pages 191-198
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSEffects of (4R)-hexahydro-7, 7-dimethyl-6-oxo-1, 2, 5-dithiazocine-4-carboxylic acid (SA 3443) on acetaminophen-induced liver injury were investigated in BALB/c mice. SA3443 (30-300 mg/kg, p.o.) dose-dependently suppressed the elevation of serum transaminase activities and the histological changes of liver induced by acetaminophen (150 mg/kg, p.o.). The compound at the same doses also reduced the mortality due to the lethal acute hepatic failure induced by acetaminophen (350 mg/kg, p.o.). Other hepatoprotective agents, cianidanol (500 mg/kg, p.o.), malotilate (100 mg/kg, p.o.), grycyrrhizine (10 mg/kg, i.p.) and cysteine (300 mg/kg, p.o.) similarly reduced it. SA3443 had no effect on glutathione (GSH) contents in the liver of normal mice, but it dose-dependently suppressed the decrease of GSH contents in the liver of BALB/c mice treated with acetaminophen. These results suggest that SA3443, a novel cyclic disulfide, provides considerable protection against acetaminopheninduced liver injury and that one of the modes of the hepatoprotective action of this compound is suppression of the decrease of GSH contents in the liver.View full abstractDownload PDF (7517K) -
Toshimitsu YAMADA, Kenichi TOMIOKA, Hideaki OKAMIYA1991 Volume 97 Issue 4 Pages 199-207
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSWe investigated the effects of YM-13650, 2-(m-carboxyacetoxyphenyl) imidazo (2, 1-b) benzothiazole, on BSA-immune complex nephritis in rats and lupus nephritis in NZB/W F1 mice. In preventative experiments on immune complex nephritis in rats, YM-13650 (10 ?? 100 mg/kg, p.o.) dose-dependently inhibited the increase in urinary protein, serum cholesterol, and urea nitrogen. Histopathological observation showed striking hypercellularity and mesangial widening in nephritic control; however, glomerular injury was reduced in YM-13650-treated animals. In therapeutic study, control rats maintained high levels of urinary protein, serum cholesterol and urea nitrogen throughout the experimental period. These variables were lower in YM 13650-treated rats. In preventative experiments in lupus mice treated from 8 weeks of age, YM 13650 in comparison with the control group showed a lesser degree of proteinuria throughout the experimental period. It also significantly prolonged or tended to prolong the life span of NZB/W F1 mice compared with the control. In therapeutic experiments conducted after the onset of lupus nephritis in mice, the drug also inhibited an increase in urinary protein and tended to prolong the life span. These results show that YM-13650 has preventative and therapeutic effects on experimental nephritis in rats and mice, and it may prove valuable as an anti-nephritic drug.View full abstractDownload PDF (6224K) -
Tetsuo AKAI, Masaya TAKAHASHI, Yukie NAKADA, Reiko OHNISHI, Yukihiro I ...1991 Volume 97 Issue 4 Pages 209-220
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSEffects of lisuride, a derivative of ergot alkaloid, on central 5-HT1A receptors were investigated biochemically, behaviorally and electroencephalographically (EEG) in rats and rabbits. Effects of lisuride in water-lick conflict tests were also investigated in rats. Lisuride was found to strongly inhibit the bindings of (3H) 8-OH-DPAT to 5-HT1A receptors in the raphe nucleus, hippocampus, cortex, amygdala and hypothalamus of rat brain. Inhibitory effects of lisuride on bindings of (3H)8-OH-DPAT in the hippocampus was almost the same as that of 5-HT (Ki = 0.5 nM) and stronger than those of the 5-HT agonist 5-MeO-DMT (Ki = 2.1 nM) or other ergot derivatives (bromocriptine and pergolide, Ki=3.0 nM). Lisuride (0.01 ?? 0.5 mg/kg, i.p.), like 8-OH-DPAT, dose-dependently induced a 5-HT behavioral syndrome in rats. Lisuride affected locomotor activity in rats, whereas 8-OH-DPAT did not. In hippocampal EEG of rabbits, lisuride (0.01 ?? 0. 03mg/kg, i.v.), like 8-OH-DPAT and diazepam, dosedependently inhibited rhythmical slow activity (RSA) induced by acoustical stimulation (3100 Hz) and also inhibited the RSA increased by administration of anxiogenic FG7142. In water-lick conflict tests, lisuride (0.05 ?? 0.1 mg/kg, i.p.), like diazepam, increased the number of shocks. These findings indicated that lisuride acts as a strong agonist on central 5-HT1A receptors and suggested that lisuride might be a potential anxiolytic.View full abstractDownload PDF (7990K) -
Hiromu KAWASAKI, Koichiro TAKASAKI1991 Volume 97 Issue 4 Pages 221-229
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe electroencephalographic (EEG) effects of rolipram were investigated in rabbits with chronic electrode implants. Intravenous administration of rolipram at 10 to 100 μg/kg evoked an increase in the arousal EEG pattern period (low amplitude fast waves) in the cortical EEG and synchronization of the hippocampal theta waves with increased voltages. Rolipram at higher doses caused behavioral excitation in rabbits. Rolipram did not affect EEG arousal responses to both auditory stimulation (2000 Hz, monotone) and electrical stimulation (100 Hz, 0.1 msec, 3-6 V) of the midbrain reticular formation or the posterior hypothalamus. The recruiting response induced by centromedian thalamic stimulation at a low frequency (7 Hz, 0.1 msec, 4-8 V) was not altered by rolipram. Rolipram was without effect on the photic driving response to flash light (2 Hz) in the occipital cortex. Rolipram caused a slight increase in the duration of afterdischarges induced by electrical stimulation (50 Hz, 0.5 msec, 4-20 V) of the dorsal hippocampus. These results suggest that rolipram is a drug that causes the EEG arousal pattern.View full abstractDownload PDF (5883K) -
Mamoru HATA, Tomoko FUJII1991 Volume 97 Issue 4 Pages 231-239
Published: 1991
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe effect of an intermittent administration of kainic acid on the KA-induced behavior, scratching, wet-dog shakes and limbic seizures was studied in the rat. Nine mg/kg kainic acid was injected i.p. at 3, 7, 14 or 21 days after the priming with the same dose of kainic acid at 25 days of age. There was no significant effect of KA-priming on the onset time of scratching. The frequency of wet-dog shakes decreased significantly in all the KA-primed rats. Fourteen day-priming of kainic acid was most effective for reducing the wet-dog shakes response. The onset time of limbic seizures tended to be shorter in all the KA-primed groups; seven day-priming resulted in a significant decrease. Histological findings showed a delay in the formation of dendritic processes of pyramidal cells in the CA3 area of the hippocampus. The results indicated that an intermittent administration of kainic acid with an interval of 3 to 21 days induces a marked tolerance in the wet-dog shakes response to kainic acid in juvenile rats, while no change in the scratching and an acceleration of the onset of limbic seizures were shown, implying that different neuronal systems are involved in these three behaviors induced by kainic acid.View full abstractDownload PDF (8535K)
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