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Biomedical subjects

H Katsuki

Publications and source records attributed to H Katsuki.

At least 73 records · Page 4Linked to original sources
PubMed1994

3,5,3'-L-triiodothyronine promotes survival and axon elongation of embryonic rat septal neurons.

The effect of 3,5,3'-L-triiodothyronine (T3) on survival and morphology of primary cultured neurons of the fetal rat brain was studied. In defined conditions of serum-free culture media we found the death preventing effect of T3 in all tested neuronal populations cultivated at high initial densities of plating (10(5) cells/cm2). While the survival of cerebrocortical neurons was improved very slightly, the number of surviving hippocampal and septal neurons reached 127.2 +/- 2.0% or 134.8 +/- 12.3% of their respective controls. The septal neurons responded at normal physiological concentration of T3 (1 nM) in high density as well as in low density cultures (5 x 10(3) cells/cm2). Moreover the treatment with 10 nM of T3 caused significant extension of the axon elongation of septal neurons (194.5 +/- 15.7%). These findings suggest the direct positive effect of T3 on pure cell population of septal neurons derived from embryonic rat brain and support the evidence for the role of this peripheral hormone during neuritogenesis.

Animals↗
PubMed1994

Arachidonic acid: toxic and trophic effects on cultured hippocampal neurons.

Arachidonic acid (20:4) is a component of membrane lipids that has been implicated as a messenger both in physiological and pathophysiological processes, including ischemic injury and synaptic plasticity. In order to clarify direct trophic or toxic effects of arachidonic acid on central neurons, primary cultures of rat hippocampal neurons were exposed to arachidonic acid under chemically-defined conditions. Arachidonic acid present in the culture medium at concentrations over 5 x 10(-6) M showed profound toxicity, whereas at lower concentrations (10(-6) M) it significantly supported the survival of hippocampal neurons. These effects were not mimicked by oleic acid (18:1) or palmitic acid (16:0). The toxic action of 10(-5) M arachidonic acid was markedly and significantly prevented by a lipoxygenase inhibitor nordihydroguaiaretic acid (10(-6) M). AA861 and baicalein (each at 10(-6) M), a selective inhibitor for 5- and 12-lipoxygenase, respectively, also showed a significant protective effect, whereas cyclooxygenase inhibitor indomethacin (10(-5) M) had no effect. The toxic action was also prevented by an antioxidant alpha-tocopherol (10(-6) M), but not by superoxide dismutase (100 U/ml) or catalase (200 U/ml). The trophic effect of 10(-6) M arachidonic acid was not suppressed by the treatments listed above. At lower concentrations (10(-7)-10(-6) M), arachidonic acid promoted neurite elongation, which was not inhibited by nordihydroguaiaretic acid or indomethacin. Overall, arachidonic acid has both trophic and toxic actions on cultured hippocampal neurons, part of which involves its metabolism by lipoxygenases. The mechanisms and the physiological significance of these effects are discussed.

Animals↗
PubMed1994

Divergent trophic actions of glioma conditioned media on cultured rat hippocampal neurons.

Neuron-glia interaction is considered to be important for the establishment and maintenance of neuronal shape and polarity during development. Glial cells release a number of trophic factors, many of which have not been fully characterized. In the present study, the trophic influences of conditioned media (CMs) of four glioma cell lines (T98G, Hs683, AC, C6) were tested on cultured hippocampal neurons dissociated from fetal rat brain. The survival of hippocampal neurons was enhanced by C6-CM, but inhibited by T98G-CM. The elongation of neurites was remarkably potentiated by C6-CM and T98G-CM. The other two CMs had little effect on neuronal survival and neurite elongation. These results suggest that different glioma cell lines produce and release different kinds and/or amounts of neurotrophic factors. Our experimental method may provide a suitable assay system for the identification of unknown trophic factors.

Animals↗
PubMed1993

Pharmacological characteristics of GABAA responses in postnatal suprachiasmatic neurons in culture.

The suprachiasmatic nucleus (SCN) is considered to be an endogenous circadian pacemaker. Previous studies have suggested functional roles of gamma-aminobutyric acid (GABA) in the control of circadian rhythms. In this study, the responses to applied GABA in cultured SCN neurons dissociated from postnatal rat hypothalamus were investigated using whole-cell voltage-clamp techniques. GABA and muscimol induced a large current response (EC50 values 5.3 and 1.6 microM, respectively), which was blocked by the GABAA antagonist bicuculline. This current response was also blocked by Zn2+ (0.5-50 microM) in a concentration-dependent manner, but was not potentiated by diazepam (10 microM) or ethanol (21 mM). These characteristics seem to correspond to those of GABAA receptors that lack gamma-type subunits.

Animals↗
PubMed1993

Synergism of tocopherol and ascorbate on the survival of cultured brain neurones.

The effects of antioxidants tocopherols and ascorbic acid were tested on the survival of hippocampal and striatal neurones in dissociated culture. Alpha- and gamma-tocopherol increased the number of surviving neurones in a concentration-dependent manner. Significant effect was observed at concentrations of 10(-8)-10(-6) M. Furthermore, the promoting effect of alpha-tocopherol on neuronal survival was markedly enhanced in the presence of ascorbic acid (2 x 10(-6) M). These results indicate that tocopherols and ascorbic acid support the survival of cultured neurones by protecting them from oxidative attack.

Animals↗
PubMed1992

The involvement of muscarinic, beta-adrenergic and metabotropic glutamate receptors in long-term potentiation in the fimbria-CA3 pathway of the hippocampus.

Possible modulatory actions of endogenous neurotransmitters on long-term potentiation (LTP) were investigated in the fimbria-CA3 pathway of rat hippocampal slices. Bath application of atropine (10 microM), but neither timolol (10 microM) nor D,L-2-amino-3-phosphonopropionate (AP3, 100 microM), significantly attenuated LTP induced by 20 pulses of 50 Hz stimulation. When stronger stimulation (3 trains of 100 Hz, 100 pulses) was used for the induction of LTP, timolol significantly attenuated LTP, but atropine and AP3 did not. These results suggest that, under specified conditions, endogenous acetylcholine through muscarinic receptors, and noradrenaline through beta-adrenergic receptors may modulate the generation of LTP in the fimbria-CA3 pathway. Metabotropic glutamate receptors may be involved not in the generation of LTP but in low-frequency synaptic transmission, since 300-1,000 microM AP3 greatly reduced, or abolished synaptic transmission in this pathway.

Adrenergic beta-Antagonists↗
PubMed1992

Involvement of postsynaptic G proteins in hippocampal long-term potentiation.

The possible involvement of postsynaptic guanosine 5-triphosphate (GTP)-binding proteins (G proteins) in long-term potentiation (LTP) was studied in rat hippocampal slices, using whole-cell recording techniques. The inclusion of guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) or guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) in the recording pipette significantly reduced or abolished the baclofen-induced hyperpolarization of pyramidal neurons, which indicates uncoupling of the signal transduction from G protein-coupled receptors by these compounds. Both GDP beta S and GTP gamma S significantly attenuated the magnitude of LTP in the fimbria-CA3 synapses, but not in the mossy fiber-CA3 synapses. GTP gamma S did not attenuate LTP in the Schaffer-CA1 synapses. The effects of guanine nucleotide analogs on fimbrial LTP were reversed by postsynaptic depolarization during high frequency stimulation. These results suggest that postsynaptic G proteins may be involved in the generation of LTP in the fimbrial synapses, possibly by affecting membrane depolarization during high frequency afferent activation.

Animals↗
PubMed1992

Possible physiological roles of aspartase, NAD- and NADP-requiring glutamate dehydrogenases of Pseudomonas fluorescens.

The levels of aspartase, NADP- and NAD-requiring glutamate dehydrogenases (GDHs) in Pseudomonas fluorescens grown under various nutritional conditions were determined. NADP-GDH showed the highest value on glucose-ammonium sulfate medium and markedly lower values on amino-acid and casamino-acids media, while the reverse was found for the NAD-GDH, as in the case of other microorganisms with two GDHs. Aspartase did not show a marked variation between the media examined. Glucose nutritionally induced NADP-GDH but suppressed NAD-GDH; and it had no effect on aspartase, which was slightly induced by casamino acids. Transfer of the cells grown on glucose-ammonium sulfate medium to casamino-acids medium clearly increased the levels of NAD-GDH and aspartase, while addition of chloramphenicol to the media abolished the increases, suggesting that the increases were due to de novo synthesis of the enzyme proteins. These results indicate that the aspartase of this microorganism has a different function from those in others, including Escherichia coli.

Amino Acids↗
PubMed1992

YM-14673, a new thyrotropin-releasing hormone analog, augments long-term potentiation in the mossy fiber-CA3 system of guinea pig hippocampal slices.

Effects of a new thyrotropin-releasing hormone (TRH) analog, N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]L-histidyl-L-prolinamide dihydrate (YM-14673), which improves experimentally induced memory dysfunction, on long-term potentiation (LTP) in the mossy fiber-CA3 system, were investigated using guinea pig hippocampal slices. At concentrations of 10(-7) M and 10(-6) M, YM-14673 significantly augmented LTP in a concentration dependent manner. The magnitude of effect of 10(-6) M YM-14673 was similar to that of 10(-6) M TRH. As LTP in the hippocampus is regarded as an elementary process of memory and learning, the augmenting effect of YM-14673 on LTP in the present study may contribute to this drug's ability to remedy memory dysfunction.

Animals↗
PubMed1991

Effects of thyrotropin-releasing hormone and a related analog, CNK-602A, on long-term potentiation in the mossy fiber-CA3 pathway of guinea pig hippocampal slices.

The effects of thyrotropin-releasing hormone (TRH) and a related analog, CNK-602A, that induces the release of catecholamines, on long-term potentiation (LTP) of the population spike in mossy fiber-CA3 pathways were investigated in guinea pig hippocampal slices. TRH augmented LTP of the population spike at concentrations of 10(-6)-10(-5) M. CNK-602A also augmented LTP at concentrations of 10(-6)-10(-5) M in a dose-dependent manner. LTP in slices of the hippocampus obtained from animals given 6-hydroxydopamine (6-OHDA) intraventricularly was significantly lower than that in non-treated animals. However, both TRH and CNK-602A (10(-6) M) augmented LTP in slices from 6-OHDA-treated animals. These findings suggest that TRH and CNK-602A augment LTP in the mossy fiber-CA3 pathway without activating noradrenergic and/or dopaminergic fibers.

Animals↗
PubMed1991

Separate mechanisms of long-term potentiation in two input systems to CA3 pyramidal neurons of rat hippocampal slices as revealed by the whole-cell patch-clamp technique.

Excitatory synaptic transmission from two input systems to hippocampal CA3 pyramidal neurons was investigated by the whole-cell patch-clamp technique for thin slice preparation, with special reference to long-term potentiation (LTP) in these systems. Excitatory postsynaptic currents (EPSCs) evoked by fimbrial stimulation consisted of two components; one was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the other was persistent at depolarized membrane potentials and blocked by D-2-amino-5-phosphonovalerate (D-AP5). The contribution of the D-AP5-sensitive component to EPSCs evoked by stimulation of mossy fibers was much less than that to fimbrial EPSCs. High-frequency stimulation of afferent fibers, under current-clamp conditions, elicited LTP. Bath application of D-AP5 blocked the induction of LTP in the fimbrial but not in the mossy fiber synapses. Induction of fimbrial LTP was completely blocked by 10 mM BAPTA applied intracellularly. In contrast, mossy fiber LTP was not blocked by 10 mM BAPTA. Furthermore, mossy fiber LTP, but not fimbrial LTP, was elicited by high-frequency stimulation under voltage-clamp (-80 mV) conditions. These results suggest that activation of NMDA receptors, increase in postsynaptic [Ca2+]i, and postsynaptic membrane depolarization are required for the induction of fimbrial but not for mossy fiber LTP.

2-Amino-5-phosphonovalerate↗
PubMed1991

Smoking and health: a review prepared by the Smoking and Health Subcommittee of the Tobacco Industries Council, a council formed by the Minister of Finance of Japan.

Any definition of health is inevitably broad and contains various elements that may differ from one individual to another. Recent studies on the effects of smoking on physical and mental health have progressed remarkably and have great value in the fields of epidemiology, pathology, clinical medicine, and psychiatry. This report concludes that while smoking may have beneficial psychological effects on smokers, it may pose a risk to physical health.

Adolescent↗
PubMed1990

Interleukin-1 beta inhibits long-term potentiation in the CA3 region of mouse hippocampal slices.

The effect of recombinant human interleukin 1-beta (IL-1 beta) on long-term potentiation (LTP) in the mossy fiber-CA3 pathway of mouse hippocampal slice preparations was investigated. IL-1 beta significantly inhibited LTP in concentrations as low as 2.9 pM (50 pg/ml). This effect of IL-1 beta was blocked by concurrent application of 100 nM Lys-D-Pro-Thr, a tripeptide analogue of IL-1 beta. This is the first evidence that IL-1 beta can regulate LTP of synaptic transmission in the hippocampus.

Animals↗
PubMed1990

Different drug-susceptibilities of long-term potentiation in three input systems to the CA3 region of the guinea pig hippocampus in vitro.

The susceptibilities to several drugs of long-term potentiations in the three input systems (mossy, commissural/associational and fimbrial fibres) to CA3 pyramidal neurones were investigated in hippocampal slices from the guinea pig. D-2-Amino-5-phosphonovalerate (D-APV), a selective antagonist at N-methyl-D-aspartate (NMDA) receptors, blocked the long-term potentiations in the commissural/associational fibre- and fimbrial fibre-CA3 systems, but did not significantly affect that in the mossy fibre-CA3 system. The latter was suppressed by kynurenate, a non-selective glutamate receptor antagonist. On the other hand, naloxone, an opioid antagonist, inhibited and bifemelane, which improves metabolism in brain and has an anti-amnesic action, augmented long-term potentiation in mossy fibre-CA3 system but did not influence those in commissural/associational fibre- and fimbrial fibre-CA3 systems. These findings suggest that the mechanisms, relevant to production of long-term potentiation in the mossy fibre-CA3 system, are different from those in the commissural/associational fibre- and fimbrial fibre-CA3 systems. N-Methyl-D-aspartate receptors are involved in the latter systems, while non-NMDA receptors for L-glutamate and opioid receptors are involved in the former. Further, the mossy fibre-CA3 system is more susceptible to a drug, having an anti-amnesic action, than are the other two systems.

2-Amino-5-phosphonovalerate↗
PubMed1989

Idebenone and vinpocetine augment long-term potentiation in hippocampal slices in the guinea pig.

The effects of idebenone and vinpocetine which reportedly prevent impairment of learning and memory were studied in vitro, on the long-term potentiation of the population spike in the pyramidal layer of CA3 region of slices of hippocampus in the guinea pig. Idebenone (10(-9) M-10(-6) M) or vinpocetine (10(-7) M-10(-6) M) significantly augmented long-term potentiation in the mossy fibre-CA3 pyramidal cell system, without any significant changes in population spikes in the absence of tetanic stimulation. These results suggest that both drugs have direct actions on the hippocampal neurones to augment long-term potentiation at fairly small concentrations. Further, when the two drugs were applied together, the augmenting effects were additive.

2-Amino-5-phosphonovalerate↗
PubMed1989

Isolation and characterization of an Escherichia coli mutant having temperature-sensitive farnesyl diphosphate synthase.

The screening of a collection of highly mutagenized strains of Escherichia coli for defects in isoprenoid synthesis led to the isolation of a mutant that had temperature-sensitive farnesyl diphosphate synthase. The defective gene, named ispA, was mapped at about min 10 on the E. coli chromosome, and the gene order was shown to be tsx-ispA-lon. The mutant ispA gene was transferred to the E. coli strain with a defined genetic background by P1 transduction for investigation of its function. The in vitro activity of farnesyl diphosphate synthase of the mutant was 21% of that of the wild-type strain at 30 degrees C and 5% of that at 40 degrees C. At 42 degrees C the ubiquinone level was lower (66% of normal) in the mutant than in the wild-type strain, whereas at 30 degrees C the level in the mutant was almost equal to that in the wild-type strain. The polyprenyl phosphate level was slightly higher in the mutant than in the wild-type strain at 30 degrees C and almost the same in both strains at 42 degrees C. The mutant had no obvious phenotype regarding its growth properties.

Alkyl and Aryl Transferases↗
PubMed1989

Indeloxazine augments long-term potentiation in the mossy fiber-CA3 system of guinea pig hippocampal slices.

The effects of indeloxazine and piracetam, which reportedly prevent experimental impairments of memory and learning, on long-term potentiation (LTP) of the population spike in the mossy fiber-CA3 system were studied in vitro using the guinea pig hippocampal slices. Indeloxazine (10(-6) M) or piracetam (10(-4) M) significantly augmented the LTP and the effect of indeloxazine on the LTP was approximately 100 times as potent as that of piracetam.

Animals↗