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A Baba

Publications and source records attributed to A Baba.

At least 145 records · Page 8Linked to original sources
PubMed1996

[Na+ -Ca2+ exchanger].

Na+ -Ca2+ exchanger couples the translocation of Na+ in one direction with that of Ca2+ in the opposite direction, and it is considered to have an important role in Ca2+ homeostasis in several cells. There are two types of Na+ -Ca2+ exchangers (cardiac and rod outer segment types). The cardiac clone (NCX1) is modeled to have an amino-terminal cleaved signal sequence, 11 transmembrane segments, and a large hydrophilic cytoplasmic domain. Several isoforms generated by alternative splicing of NCX1 and an isoform (NCX2), a product of a different gene, are present in different tissues. This brief review focuses on the physiological importance, molecular aspects and the pathological roles of the exchanger, especially NCX1.

Amino Acid Sequence↗
PubMed1996

The value of positive nitrites in screening asymptomatic bacteriuria amongst Malaysian school children.

It is important to diagnose and treat urinary tract infection in children before renal damage has taken place. Hence a new screening procedure will be of interest. This study was conducted to evaluate the efficacy of urinary nitrite in screening for asymptomatic bacteriuria among school children compared to a more traditional method. Of the 44,816 school children investigated 240 (0.54%) students were judged to have bacteriuria ie 82 (0.19%) in boys and 158 (0.35%) in girls. Escherichia coli was the commonest organism isolated (28.75%). Urine dipstick testing for nitrite was found to have a low sensitivity and positive predictive value. While urinalysis for pyuria was noted to have a sensitivity of 77.9%, a specificity of 95.8% and a negative predictive value of 99.9%.

Bacteriuria↗
PubMed1995

Structure of the gene encoding the mouse pituitary adenylate cyclase-activating polypeptide receptor.

The PACAP-R gene, encoding the mouse pituitary adenylate cyclase-activating polypeptide receptor (PACAP-R), has been isolated and its structural organization has been determined. PACAP-R spans more than 50 kb and is divided into 18 exons. PACAP-R contains two alternative exons encoding the putative third intracellular loop, as found in the rat PACAP-R. The proximal promoter region is highly G+C rich and lacks an apparent TATA box, but contains a CCAAT box and two potential Sp1-binding sites.

Animals↗
PubMed1995

Antidepressant-like effect by postsynaptic 5-HT1A receptor activation in mice.

The antidepressant-like effect of 5-(3(-)[((2S)-1,4-benzodioxan-2-ylmethyl)amino]propoxy)-1,3- benzodioxole (MKC-242), a novel 5-HT1A receptor agonist, was studied in the forced swimming test in mice injected i.c.v. with 5,7-dihydroxytryptamine to destroy 5-HT neurons or treated with p-chlorophenylalanine to inhibit 5-HT synthesis. MKC-242 reduced immobility time of mice pretreated with vehicle and these drugs, although it did not affect their locomotor activity. The anti-immobility effect was antagonized by 5-HT1A receptor antagonists such as propranolol and N-tert-butyl-3-(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenylpropana mide. These findings support the hypothesis that postsynaptic 5-HT1A receptors play an important role in the antidepressant-like effect of 5-HT1A receptor agonists.

5,7-Dihydroxytryptamine↗
PubMed1995

Expression of glutamate transporters in cultured glial cells.

Expression of mRNAs for glutamate transporter (GLT-1) and glutamate aspartate transporter (GLAST) was investigated in three different types of purified glial cells by the reverse transcriptase-polymerase chain reaction (RT-PCR). Cultured astrocytes, oligodendrocytes, and microglia expressed mRNAs for GLAST and GLT-1; mRNA for GLAST was expressed more prominently than that for GLT-1 in astrocytes. Oligodendrocytes and microglia expressed mRNAs for both GLT-1 and GLAST equally, but the expression in microglia was not prominent, suggesting glutamate uptake is not essential in microglia. In astrocytes cultured from different brain regions, GLAST mRNA was equally expressed. GLT-1 mRNA was also detected in these astrocytes, but the expression level was lower than that of GLAST.

ATP-Binding Cassette Transporters↗
PubMed1995

cDNA cloning of a thromboxane A2 receptor from rat astrocytes.

A cDNA clone for rat thromboxane (TX) A2 receptor was obtained from cultured astrocytes. The cDNA encodes a protein of 341 amino acids with seven putative transmembrane domains. The receptor is homologous with mouse and human TXA2 receptors at 92.7% and 71.8%, respectively. Expression of messenger RNA for the receptor was examined by reverse transcriptase-polymerase chain reaction, showing ubiquitous expression in brain glial cells such as astrocytes, oligodendrocytes and microglia.

Amino Acid Sequence↗
PubMed1995

NE-100, a novel sigma ligand: effects on [3H]TCP binding to intact primary cultured neuronal cells.

N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-ethylamine monohydrochloride (NE-100), a potent and highly selective sigma ligand, haloperidol, (+)pentazocine, 1-(cyclopropyl-methyl)-4-(2'-(4"-fluorophenyl)-2'-oxoethyl) piperidine HBr (DuP 734) and 4-(2'-(4"-cyanophenyl)-2'-oxoethyl) 1-(cyclopropylmethyl)piperidine (XJ 448) inhibited carbachol-induced inositol 1,4,5-triphosphate (IP3) formation in a dose-dependent manner. The rank order of potency of the tested drugs for inhibition was: haloperidol > or = (+)pentazocine = NE-100 > DuP 734 = XJ 448. In addition, the effects of NE-100, DuP 734 and XJ 448 upon [3H]TCP binding were examined using primary cultured neuronal cells derived from the fetal rat telencephalon. These drugs inhibited [3H]TCP binding to intact cells. The ability of the test drugs to inhibit [3H]TCP binding to primary cultured neuronal cells was in the order: NE-100 > DuP 734 > XJ 448. These observations suggest that NE-100 indirectly modulates the N-methyl-D-aspartate (NMDA)/phencyclidine (PCP) receptor ion channel complex (NMDA receptor-ion channel), presumably through sigma-1 sites.

Animals↗
PubMed1995

Intracellular ascorbic acid inhibits the Na(+)-Ca2+ exchanger in cultured rat astrocytes.

The effect of ascorbic acid on Ca2+ uptake in cultured rat astrocytes was examined in the presence of ouabain and monensin, which are considered to drive the Na(+)-Ca2+ exchanger in the reverse mode. Ascorbic acid at 0.1-1 mM inhibited Na(+)-dependent Ca2+ uptake significantly but not Na(+)-dependent glutamate uptake in the cells, although the inhibition required pretreatment for more than 30 min. The effect of ascorbic acid on the Ca2+ uptake was blocked by simultaneous addition of ascorbate oxidase (10 U/ml). Na(+)-dependent Ca2+ uptake was also inhibited by isoascorbate at 1 mM but not by ascorbate 2-sulfate, dehydroascorbate, and sulfhydryl-reducing reagents such as glutathione and 2-mercaptoethanol. The inhibitory effect of ascorbic acid was observed even in the presence of an inhibitor of lipid peroxidation, o-phenanthroline, or a radical scavenger, mannitol, and the degrading enzymes such as catalase and superoxide dismutase. On the other hand, the inhibitory effect was not observed under the Na(+)-free conditions that inhibited the uptake of ascorbic acid in astrocytes. When astrocytes were cultured for 2 weeks in a medium containing ascorbic acid, the content of ascorbic acid in the cells was increased and conversely Na(+)-dependent Ca2+ uptake was decreased. These results suggest that an increase in intracellular ascorbic acid results in a decrease of Na(+)-Ca2+ exchange activity in cultured astrocytes and the mechanism is not related to lipid peroxidation.

Animals↗
PubMed1995

Nitroprusside and cyclic GMP stimulate Na(+)-Ca2+ exchange activity in neuronal preparations and cultured rat astrocytes.

The effects of nitric oxide (NO)-generating agents on 45Ca2+ uptake in rat brain slices and cultured rat astrocytes were studied in the presence of monensin, which is considered to drive the Na(+)-Ca2+ exchanger in the reverse mode. Sodium nitroprusside (SNP) at > 10 microM increased monensin-stimulated Ca2+ uptake in the slices, although it did not affect high K(-)-stimulated Ca2+ uptake. Another NO donor, 3-morpholinosydnonimine, was effective. The effect of SNP was antagonized by hemoglobin (50 microM), a NO scavenger, and mimicked by 8-bromo-cyclic GMP (100 microM). In rat brain synaptosomes, SNP increased monensin-stimulated Ca2+ uptake, but it did not affect high K(+)-stimulated Ca2+ uptake. 8-Bromocyclic GMP, but not SNP, increased Na(+)-dependent Ca2+ uptake significantly in synaptic membrane vesicles in the absence of monensin. In cultured rat astrocytes, SNP and 8-bromo-cyclic GMP increased Ca2+ uptake in the presence of ouabain and monensin, which were required for the Ca2+ uptake in the cells. These findings suggest that NO stimulates the Na(+)-Ca2+ exchanger in neuronal preparations and astrocytes in a cyclic GMP-dependent mechanism.

Animals↗
PubMed1995

Increase in chloride-dependent L-glutamate transport activity in synaptic membrane after in vitro ischemic treatment.

The effect of energy failure on Cl(-)-dependent L-glutamate (L-Glu) transport was examined with an in vitro preparation. Rat brain slices were incubated in low oxygen and glucose-deprived medium (in vitro ischemia), and a synaptic membrane fraction was prepared from the slices. Cl(-)-dependent L-[3H]Glu uptake into vesicles increased about twofold after 20 min of in vitro ischemia. The increased L-[3H]Glu uptake was inhibited by L-Glu, DL-2-amino-4-phosphonobutyrate, L-homocysteic acid, L-cystine, 4,4'-diisothiocyano-2,2'-disulfonic stilbene, and removal of Cl-. Uptakes of Na(+)-dependent L-[3H]Glu, [3H]GABA, and [3H]taurine were not changed by the in vitro ischemia. In vitro ischemia increased the Vmax value without affecting the Km value. The increased L-[3H]Glu uptake by in vitro ischemia was reduced by subsequent incubation in a normoxic glucose-containing solution. ATP content in brain slices decreased to < 10% of control values by in vitro ischemia for 10 min. The decrease in ATP content was restored by subsequent incubation in normoxic glucose-containing solution. Treatment with veratrine, 2,4-dinitrophenol, carbonyl cyanide m-chlorophenylhydrazone, and NaCN in normoxic conditions increased L-[3H]Glu uptake with a concomitant decrease in ATP content in slices. These results suggest that Cl(-)-dependent L-Glu transport activity in synaptic membranes increases in ischemia- or hypoxia-induced brain energy failures.

ATP-Binding Cassette Transporters↗
PubMed1995

Increase of noradrenaline release in the hypothalamus of freely moving rat by postsynaptic 5-hydroxytryptamine1A receptor activation.

1. 5-Hydroxytryptamine (5-HT) plays a role in the regulation of noradrenergic neurones in the brain, but the precise mechanism of regulation of noradrenaline (NA) release by 5-HT1A receptors has not been defined. The present study describes the effect of a highly potent and selective 5-HT1A receptor agonist, 5-(3-[[(2S)-1,4-benzodioxan-2-ylmethyl)]amino]propoxy)-1,3-b enzodioxole HC1 (MKC-242), on NA release in the hypothalamus using microdialysis in the freely moving rat. 2. Subcutaneous injection of MKC-242 (0.5 mg kg-1) increased extracellular levels of NA and its metabolite, 3-methoxy-4-hydroxyphenylglycol, in the hypothalamus and hippocampus. 3. The 5-HT1A receptor agonists, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) (0.2 mg kg-1) and buspirone (3 mg kg-1) mimicked the effect of MKC-242 in increasing NA release in the hypothalamus. 4. The effects of MKC-242 and 8-OH-DPAT in the hypothalamus were antagonized by pretreatment with WAY100135 (10 mg kg-1), a silent 5-HT1A receptor antagonist. 5. Local administration of 8-OH-DPAT (10-100 microM), citalopram (1 microM), a 5-HT reuptake inhibitor, and MDL72222 (10 microM), a 5-HT3 receptor antagonist, into the hypothalamus, had no effect on NA release. 6. Intracerebroventricular injection with 5,7-dihydroxytryptamine caused a marked reduction in brain 5-HT content, but the treatment affected neither basal NA levels nor the MKC-242-induced increase in NA release. 7. The effect of MKC-242 in increasing NA release was not attenuated by repeated treatment with the drug (0.5 mg kg-1, once a day for 2 weeks). 8. The present results suggest that activation of postsynaptic 5-HT1A receptors increases NA release in the hypothalamus.

5,7-Dihydroxytryptamine↗
PubMed1995

Fluid and protein secretion by the submandibular glands of weanling rats in response to cholinergic and peptidergic agonists at various doses.

Fluid and protein secretion by the submandibular glands of 25-day-old rats were examined and compared in response to three cholinergic and four peptidergic sialogogues at various doses. All cholinergic and peptidergic agonists used were potent sialogogues for the submandibular glands of the weanling rats over the wide range of doses used. The cholinergic agonists, bethanechol and methacholine and the peptidergic agonists, substance P, substance PTyr8 and eledoisin-related peptide used intravenously, acted similarly to each other on the submandibular glands of the rats, late in the natural weaning period, but carbachol and physalaemin had slightly different effects. Of the peptidergic agonists, physalaemin was the most potent sialogogue among four tachykinins tested at the low dose. The types of protein secreted by the submandibular glands of the weanling rats in response to all sialogogues used here were typical of the beta-type. These results indicate that all agonists used could mainly stimulate the acinar cells of the submandibular glands of the weanling rats which have already fully developed functionally at this time.

Animals↗
PubMed1995

Inhibitory effect of ginseng total saponins on glutamate-induced swelling of cultured astrocytes.

The effects of ginseng total saponins (GTS) on L-glutamate-induced swelling of cultured astrocytes from rat brain were studied. Following exposure to 0.5 mM glutamate for 1 h, the intracellular water space (as measured by [3H]O-methyl-D-glucose uptake) of astrocytes increased three-fold with a morphological change: the disappearance of cellular processes. Simultaneous addition of GTS with glutamate reduced the astrocytic swelling in a dose-dependent manner. GTS at 0.5 mg/ml did not affect the viability of astrocytes for up to 18 h, which was determined by a colorimetric assay for cellular growth and survival. These data suggest that GTS prevents the cell swelling of astrocytes induced by glutamate.

Animals↗
PubMed1995

Stimulation of cyclic AMP formation by pituitary adenylate cyclase-activating polypeptide is attenuated by glutamate in rat brain slices.

In rat hippocampal slices, pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) stimulated cyclic AMP formation in dose- and time-dependent manners. The PACAP-38 action was dose-dependently attenuated by L-glutamate in the hippocampus; L-glutamate at the concentration of 1 mM attenuated PACAP-38-stimulated cyclic AMP formation by approximately 30%. The inhibitory effect of L-glutamate is also observed in rat cerebellar slices. In contrast, the inhibitory effect of a prostanoid EP3-receptor agonist on PACAP-38-stimulated cyclic AMP formation was brain region-specific; the inhibitory action was observed in the cerebellum but not in the hippocampus.

Adenylyl Cyclases↗
PubMed1995

Effects of serotonin1A agonists on anoxia-induced impairment of protein synthesis in rat brain slices.

Earlier in vivo experiments suggest that serotonin1A (5-HT1A) agonists are new tools for the treatment of experimental cerebral ischemia. The present study examined this idea in an in vitro system. Incubation of rat brain slices under anoxic conditions for 30 min decreased protein synthesis that was assayed in a normoxic medium by measuring the incorporation of [14C]lysine into trichloroacetic acid-insoluble tissue extracts. The 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino) tetralin (10-100 microM) and buspirone (50 microM) attenuated the anoxia-induced decrease in protein synthesis in the slices. Although the degree of the effect is small, it may be relevant to the neuroprotective effect in the in vivo experiments.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

DA1 receptor-mediated renin release from isolated rat glomeruli.

The present study was performed in order to examine the effects of dopamine (DA) on renin release and to clarify which subtype of DA receptor, DA1 or DA2 contributes to renin release. Male Wistar rats aged seven weeks were used. Glomeruli were isolated by the modified Beierwaltes' sieving method and were transferred to a sealed chamber and superfused with Krebs-Ringer solution. In the first experiment, the changes in renin release induced by DA and the effects of a non-selective DA antagonist, haloperidol and a beta antagonist, propranolol on DA-induced renin release were examined. In the second experiment, the effect of a DA2 receptors antagonist, spiperone and of a DA1 receptor antagonist, SCH-23390 on renin release were investigated. Basal levels of renin release were 2.46 +/- 0.36 ng ATI/h/10(4) glomeruli (mean +/- SEM). DA caused a dose-dependent increase in renin release. The renin release induced by DA was inhibited by haloperidol but not by propranolol. The maximum level of renin release induced by 10(-5)M DA was 4.13 +/- 0.63 ng ATI/h/10(4) glomeruli. SCH-23390 at 10(-5)M caused significant suppression of DA-induced renin (p < 0.05). In contrast, 10(-5)M spiperone failed to suppress DA-induced renin release. These results suggest that DA induced renin release from isolated glomeruli through the DA1 receptors.

Adrenergic beta-Antagonists↗
PubMed1995

Peritoneal mast cell hyperplasia in rats after IgE antibody-antigen interaction.

Peritoneal mast cell hyperplasia was investigated in rats after evoking IgE antibody-antigen reaction. Rats were immunized with antigen and then passively sensitized with monoclonal IgE antibody before antigen challenge. A significant increase in the number of peritoneal mast cells was observed 3 weeks after the antigen challenge in the peritoneal cavity, although the histamine content of the mast cells was decreased significantly. In rats without prior immunization, these changes were not observed. Stimulation with compound 48/80 or calcium ionophore A23187 did not affect the number of mast cells. This model may prove to be a useful tool for studying the mechanisms of mast cell hyperplasia and recruitment of mast cell precursors in vivo.

Animals↗