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Biomedical subjects

A Baba

Publications and source records attributed to A Baba.

At least 19 recordsLinked to original sources
PubMed1992

Sex difference for tolerance of 5-HT1A receptor-mediated temperature and corticosterone responses in mice.

Repeated treatment with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) resulted in significant attenuation of 8-OH-DPAT-induced hypothermia and adrenocorticol effect in mice of both sexes, while it did not affect the 8-OH-DPAT-induced decrease in 5-hydroxyindoleacetic acid in the hypothalamus in either sex. The attenuated responses developed more rapidly in female than in male mice, indicating sex differences in the adaptive regulation of the 5-HT1A receptor-mediated responses.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Fetal liver T cell receptor gamma/delta+ T cells as cytotoxic T lymphocytes specific for maternal alloantigens.

We have established fetal liver-derived T cell receptor (TCR) gamma/delta+, CD3+ T cell lines that are cytotoxic for maternal T cells. Fetal liver-derived lymphoid progenitors yielded predominantly TCR-gamma/delta+ cell clusters when cultured on fetal bone marrow-derived stromal cells in the presence of a cytokine cocktail under magnetic force. These tightly adherent clusters were cloned by limiting dilution and the resulting cell lines analyzed for phenotype and function. Six of eight TCR-gamma/delta lines from 8-9.5-wk gestation fetuses were V delta 2+ as compared with zero of eight lines from later stages of gestation (10 and 15 wk), where all the lines were V delta 1+. In cytotoxicity assays, these TCR-gamma/delta+, CD3+, CD4-, and CD8+ or CD8- long-term cultured lymphoid cells (LLC) were killer cells active against the class I antigens on maternal T cells. Of the cell lines, the CD8+ TCR-gamma/delta+ LLC had the highest levels of killer activity. Thus fetal liver TCR-gamma/delta+ T cells may play a crucial role in protection against invading maternal T cells generated in the feto-maternal interaction.

Cells, Cultured↗
PubMed1992

Glucose and oxygen deprivation induces a Ca(2+)-mediated decrease in (Na(+)+K+)-ATPase activity in rat brain slices.

Exposure of rat brain cortical slices to a medium lacking in glucose, oxygen or both glucose and oxygen, resulted in a decrease of the tissue ATP content and a reduction of (Na(+)+K+)-ATPase activity in membranes prepared from the slices. These treatments also inhibited partial reactions of (Na(+)+K+)-ATPase such as Na(+)-dependent phosphorylation and K(+)-stimulated phosphatase, as well as specific binding of [3H]ouabain in membranes prepared from the slices. Glucose deprivation and hypoxia decreased (Na(+)+K+)-ATPase activity in the absence of extracellular Ca2+, but the effects were blocked by 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid tetra-acetomethyl ester (BAPTA-AM), a chelator of intracellular Ca2+. Metabolic inhibitors mimicked the effects of glucose deprivation and hypoxia. The effect of glucose-free hypoxia was dependent on extracellular Ca2+. It was blocked by Mg2+ at high concentration, bepridil or amiloride, but not by voltage-sensitive Ca2+ channel antagonists and glutamate receptor antagonists. None of the drugs tested here, except for dithiothreitol, affected the inhibitory effect of glucose-free hypoxia on the enzyme activity. In contrast to brain (Na(+)+K+)-ATPase, the kidney enzyme was insensitive to glucose and oxygen deprivation and metabolic inhibitors which depleted the tissue ATP.

Animals↗
PubMed1992

Effects of long-term anticonvulsant therapy on copper, zinc, and magnesium in hair and serum of epileptics.

The effects of long-term anticonvulsant therapy on copper (Cu), zinc (Zn), and magnesium (Mg) in the serum and hair were investigated in epileptics. Hair concentrations of Cu in both male and female epileptics, Zn in male epileptics, and Mg in female epileptics were significantly decreased when compared with those of age-matched and gender-matched controls. Hair Cu concentrations were significantly decreased in male epileptics; a significant decrease in hair Mg concentration was observed in female epileptics when compared with schizophrenics. An increased serum Cu concentration was found in female epileptics and a decreased Zn concentration was found in male epileptics. These findings suggest that long-term anticonvulsant therapy could induce alterations in both the metabolism and distribution of Cu, Zn, and Mg.

Adult↗
PubMed1992

Postnatal change in a Ca(2+)-mediated decrease in (Na+ + K+)-ATPase activity in rat brain slices.

The treatment of brain slices from immature rats with veratrine and monensin did not cause any change in (Na+ + K+)-adenosine triphosphatase (ATPase) activity or [3H]ouabain binding in membranes prepared from the slices, though these reagents remarkably stimulated Ca2+ uptake in the slices. Exposure of the slices from adult rats to a glucose-free, hypoxic or both glucose-free and hypoxic medium resulted in a decrease in the enzyme activity, but the enzyme from immature rats was resistant to the conditions.

Animals↗
PubMed1992

[Regulation by chloride ion of astroglial cell functions and morphological transformation].

Recently, several lines of evidence have indicated the important roles of glial cells, especially astrocytes, in the regulation of neuronal functions. The neuron-glia interaction is one of the most important issues in neuroscience, including neuropharmacology. I reviewed the present status and perspectives on the physiologic and pathologic functions of astrocytes in relation to the roles of intracellular Cl-. Astrocytes have different types of Cl- transport systems, such as voltage-sensitive and ligand-gated channels; HCO3(-)-Cl- exchange; and Na+, K+, Cl- cotransport systems. Anion exchange and cotransport systems are responsible for intracellular pH regulation and astrocytic volume regulation, respectively. Especially, astrocytic volume regulation is physiologically important for reducing the concentrations of K+ and glutamate in the extracellular space by their uptake systems. Disturbance of astrocytic volume regulation is expressed as astrocytic swelling, which is usually observed in various brain pathologic states including ischemia. Experimentally, glutamate caused a typical swelling of astrocytes in culture by Cl- and Ca(++)-dependent processes. Glutamate-induced swelling is qualitatively different from reversible swelling induced by hypoosmotic medium. Recently, we found that Cl- is intracellular factor for modulating the receptor-adenylate cyclase system in brain slices. Similarly, the receptor- and forskolin-stimulated adenylate cyclase of astrocytes showed a clear Cl- dependence. This was functionally confirmed by astrocytic morphological transformation induced by the cyclic AMP system.

Astrocytes↗
PubMed1992

Effect of dibutyryl cyclic AMP-treatment on prostaglandin F2 alpha-stimulated phosphoinositide hydrolysis in cultured rat astrocytes.

Dibutyryl cyclic AMP (dBcAMP)-treatment of cultured rat astrocytes induced changes in astrocyte morphology followed by the potentiation of prostaglandin F2 alpha (PGF2 alpha)-stimulated phosphoinositide (PI) hydrolysis. The potentiation was observed in astrocytes of the cerebral cortex, cerebellum, and hippocampus. The dBcAMP-treatment induced agonists-specific changes in PI hydrolysis; e.g., the potentiation of norepinephrine-effect and the reduction of the carbachol-effect. Coincubations of carbachol or norepinephrine with PGF2 alpha produced additive responses.

Animals↗
PubMed1992

Mechanism of extracellular ATP-stimulated phosphoinositide hydrolysis in rat glioma C6 cells.

In rat glioma C6 cells, extracellular ATP stimulated phosphoinositide (PI) hydrolysis in concentration- and time-dependent manners with a median effective dose value of 60 microM. The maximal response was attained at 300 microM ATP. Of adenine nucleotides, ATP and adenosine 5'-O-(3-thiotriphosphate) were most effective, while adenosine, AMP and beta,gamma-methylene ATP were ineffective. Similar results were obtained in cultured rat astrocytes. The stimulatory effects of ATP and ADP were negated by removal of external Ca++ in C6 cells. ATP at 300 microM induced an elevation of intracellular Ca++ concentration in 1-[2-(5-carboxyoxazol-2-yl)-6-amino-benzofuran-5-oxy]-2-(2'-amino- 5'- methylphenoxy)-ethane-N,N,N',N' acid-loaded C6 cells. This response was not blocked by nifedipine (10 microM) and verapamil (10 microM). A Ca++ ionophore A23187 (10 microM) stimulated PI hydrolysis in C6 cells. The responses to ATP (300 microM) and A23187 (10 microM) were additive. In digitonin-permeabilized C6 cells, Ca++ at the concentration of 100 microM evoked PI hydrolysis, and ATP alone did not affect the Ca++ dependence. GTP gamma S (100 microM) stimulated the PI hydrolysis at a range of 0.1 to 10 microM Ca++, and ATP enhanced the GTP gamma S response in the permeabilized cells. These results suggest that activation of P2-purinergic receptors by ATP causes phospholipase C to be activated by subthreshold concentrations of Ca++ via GTP-binding proteins, resulting in an activation of the enzyme in response to stimulated Ca++ influx.

Adenosine Triphosphate↗
PubMed1991

Na+ influx-induced decrease of (Na+ + K+)-ATPase activity in rat brain slices: role of Ca2+.

Treatment of rat brain slices with veratrine and monensin decreased (Na+ + K+)-ATPase activity in the membranes in a dose-dependent manner. The effect of monensin, like that of veratrine, was accompanied by a decrease of maximal binding sites for ouabain. The inhibitory effect of monensin on the enzyme activity was dependent on external Ca2+ at low concentrations, but not at a high concentration. The decreased enzyme activity induced by monensin was restored by subsequent incubation of the slices in a Ca(2+)-free medium containing 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetraacetoxymethyl ester (BAPTA-AM), a chelator of intracellular Ca2+. The effect of monensin at a low concentration on enzyme activity was antagonized by amiloride (1 mM), bepridil (5 microM), quinacrine (30 microM) or verapamil (30 microM), but not by nifedipine (1 microM) or omega-conotoxin (1 microM). Furthermore, the inhibitory effect of monensin at a high concentration under Ca(2+)-free conditions was blocked by BAPTA-AM (30 microM) and by bepridil (100 microM) or diazepam (500 microM), inhibitors of mitochondrial Na(+)-Ca2+ exchange. Inhibitors of calmodulin, protein kinase C, phospholipase A2 and calpain did not affect the monensin-induced decrease of enzyme activity. Dithiothreitol (10 mM) blocked the effect of monensin on enzyme activity but did not affect the ionophore-induced influx of Ca2+ in the slices.

Amiloride↗
PubMed1991

Inhibition of NMDA-induced protein kinase C translocation by a Zn2+ chelator: implication of intracellular Zn2+.

The role of intracellular Zn2+ in the translocation of protein kinase C from cytosol to membrane fractions was examined by the [3H]phorbol 12,13-dibutyrate (PDBu) binding method in guinea pig cerebral synaptoneurosomes. N-methyl-D-aspartate (NMDA, 100 microM) and calcium ionophore A23187 (0.3-30 microM) decreased the binding activity in the cytosol with a concomitant increase in the membrane fractions. Pretreatment of synaptoneurosomes with a heavy metal chelator, N,N,N',N'-tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN), inhibited the NMDA- and A23187-induced changes of the distribution of [3H]PDBu binding sites in cytosol and membrane fractions. The inhibitory effect of TPEN was negated by a preincubation of TPEN with equimolar Zn2+ but not by that with Ca2+. The addition of 500 microM Zn2+ to the lysate of synaptoneurosomes induced an increase of [3H]PDBu binding activity in the membrane fraction with a concomitant decrease in the cytosol fraction, as did 100 microM Ca2+. Low concentrations of Zn2+ (10 microM), which alone had no effect on the distribution of the binding, significantly enhanced the effect of 10 microM Ca2+ in the lysate. Under those conditions TPEN inhibited the Zn(2+)-potentiated Ca(2+)-dependent changes in the binding. These results suggest that intracellular Zn2+ is essential for the agonist-induced translocation of protein kinase C in guinea pig synaptoneurosomes.

Animals↗
PubMed1991

Astrocytes possess prostaglandin F2 alpha receptors coupled to phospholipase C.

We examined the effect of prostaglandin (PG) F2 alpha on phosphoinositide (PI) hydrolysis in rat cultured astrocytes. PGF2 alpha stimulated the formation of [3H]inositol phosphates in [3H]inositol-labeled astrocytes with the ED50 value of 23 nM, whereas PGD2 and PGE2 were much less effective than PGF2 alpha. Transformation of astrocytes was accompanied by an increase in the stimulatory response of PGF2 alpha. Pretreatment of the astrocytes with pertussis toxin and cholera toxin did not affect the PGF2 alpha-evoked PI hydrolysis. In the digitonin-permeabilized astrocytes, PGF2 alpha significantly enhanced the GTP gamma S-evoked PI hydrolysis in the presence of Ca2+. These results indicate that rat cultured astrocytes possess PGF2 alpha receptors coupled to phospholipase C.

Animals↗
PubMed1991

Gonadectomy changes the pituitary-adrenocortical response in mice to 5-HT1A receptor agonists.

The effects of 5-HT1A receptor agonists such as 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), BP-554 and buspirone on the serum corticosterone level were significantly more pronounced in female than in male mice. A similar sex difference was observed for the effect of 8-OH-DPAT on the plasma ACTH level. Pretreatment with proadifen, an inhibitor of microsomal drug-metabolizing enzymes, did not affect the sex difference in the effect of 8-OH-DPAT. The corticosterone response to 8-OH-DPAT in female mice was attenuated by ovariectomy. The effect of 8-OH-DPAT in ovariectomized mice was enhanced by chronic estradiol and the enhancement was blocked by testosterone. In male mice the corticosterone response to 8-OH-DPAT increased at 5 weeks after castration but had not changed at 2 weeks. Chronic estradiol enhanced the corticosterone response to 8-OH-DPAT in castrated mice. There was no difference between sexes in [3H]8-OH-DPAT binding to membranes and in the contents of 5-HT and 5-hydroxyindoleacetic acid in the hypothalamus. Accumulation of 5-hydroxytryptophan after decarboxylase inhibition in the hypothalamus was however greater in female than in male mice.

5-Hydroxytryptophan↗
PubMed1991

NMDA induces protein kinase C translocation in hippocampal slices of immature rat brain.

N-Methyl-D-aspartate (NMDA)-induced translocation of protein kinase C (PKC) from cytosol to membrane fractions was examined by the methods of [3H]phorbol 12,13-dibutyrate binding and western blotting in rat hippocampal slices. NMDA and L-glutamate induced translocation of PKC from cytosol to membrane fractions in immature rat hippocampal slices, but not in mature ones. The NMDA-induced translocation of PKC was dependent on Ca2+. It was inhibited by the NMDA receptor antagonists, 2-amino-5-phosphonovaleric acid and ketamine, but not by Mg2+ and Zn2+. These results suggest that stimulation of NMDA receptors enhances Ca2+ influx and thereby induces translocation of PKC in immature rat hippocampus.

Aging↗
PubMed1991

A morphological study on glutamate-induced swelling of cultured astrocytes: involvement of calcium and chloride ion mechanisms.

Morphological changes in cultured astrocytes exposed to L-glutamate (Glu) were examined light and electron microscopically. The treatment with 0.1 mM Glu for 60 min caused marked swelling of the cells, which was characterized by reduction in staining of cytoplasm with Toluidine blue, disappearance of the cytoplasmic granular ground substances, swollen mitochondrion and nucleus, and dispersed chromatin. The above changes were prevented by the removal of Na+, Ca2+ or Cl- from the incubation medium for Glu treatment. However, the Glu treatment in a Cl(-)-free medium caused conspicuous aggregation of 10 nm filaments.

Animals↗
PubMed1991

L-glutamate-induced swelling of cultured astrocytes is dependent on extracellular Ca2+.

L-Glutamate (L-Glu)-induced swelling of astrocyte cultures from rat brain was examined by determining [3H]O-methyl-D-glucose ([3H]OMG) uptake. Time-course of the L-Glu (0.5 mM)-induced increase in [3H]OMG space of astrocytes showed two phases; about 30% increase was obtained in 10 min and the increased [3H]OMG space was steady up to 20 min. Then, the [3H]OMG space was further increased during the incubations longer than 30 min. In Ca2(+)-free conditions, while the time-course up to 20 min was similar to that in the normal condition, the increase in [3H]OMG space by further incubations was not shown. The L-Glu-increased [3H]OMG space persisted for 2 h in a L-Glu-free medium and thereafter turned to the normal level in 4 h. In contrast, the incubation in a L-Glu-free medium for 30 min reversed the increased [3H]OMG space in the absence of extracellular Ca2+. These results indicate that swelling of astrocytes induced by L-Glu is characterized by an accompanied influx of Ca2+.

3-O-Methylglucose↗
PubMed1991

Membrane-associated thiamine triphosphatase in rat skeletal muscle.

1. Thiamine triphosphatase activity in particulate fraction, but not in soluble, of rat skeletal muscle was stimulated by several anions. 2. The stimulative effect of anions was dependent on pH of reaction medium and was reversible. 3. The activities of ATPase in rat muscle particulate preparation and thiamine triphosphatase in the brain were inhibited by the anions.

Animals↗
PubMed1991

Postnatal development of thiamine metabolism in rat skeletal muscle.

1. The activities of 2-oxoglutarate dehydrogenase, transketolase, thiamine pyrophosphokinase and thiamine triphosphatase and the concentrations of thiamine phosphates were almost the same between rat extensor digitorum longus and soleus muscles at 2 weeks of age. 2. These enzyme activities changed after 3 weeks of age in a different way depending on the muscle phenotype. 3. Thiamine diphosphate level and the activity of 2-oxoglutarate dehydrogenase increased only in soleus muscle and thiamine triphosphate level increased only in extensor digitorum longus during development.

Aging↗