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S Kitayama

Publications and source records attributed to S Kitayama.

At least 73 records · Page 4Linked to original sources
PubMed1993

12-Lipoxygenase product as an inhibitor of the action of chemoattractant peptide fMet-Leu-Phe in rat neutrophils.

1. 12-Hydroxyeicosatetraenoic acid (12-HETE) has been evaluated for its capacities to modulate neutrophil migration and cytosolic Ca2+ ([Ca2+]i) using compounds prepared by chemical synthesis and tissue extract from dog gingiva. 2. 12-HETE inhibited N-formyl-Met-Leu-Phe (fMLP)-stimulated neutrophil migration in a concentration-dependent fashion. 3. The tissue extract from dog gingiva mimicked the actions of 12-HETE. 4. Although 12-HETE failed to increase [Ca2+]i, preincubation of neutrophils with 12-HETE led to a suppression of [Ca2+]i when the cells were subsequently stimulated by fMLP. 5. Again tissue extract from dog gingiva mimicked the action of 12-HETE on [Ca2+]i. 6. These results suggest the possible correlation of the inhibitory activities of 12-HETE on the regulation of neutrophil migration and Ca2+ mobilization, and this may be important for the role of 12-HETE in pathogenesis in periodontal tissues.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Dopamine transporter site-directed mutations differentially alter substrate transport and cocaine binding.

Polar amino acids lying within three hydrophobic regions of the dopamine transporter (DAT) are analogous to those important for ligand recognition by catecholamine receptors. Possible functional significance of these amino acids was examined by expressing DAT cDNAs mutated in these polar residues. Replacement of aspartate at position 79 with alanine, glycine, or glutamate dramatically reduced uptake of [3H]dopamine and the tritium-labeled Parkinsonism-inducing neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and reduced the mutants' affinity for the tritium-labeled cocaine analog (-)-2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane (CFT) without affecting Bmax. Replacement of the serine residues at positions 356 and 359 in the seventh hydrophobic region by alanine or glycine caused reductions in [3H]dopamine and [3H]MPP+ uptake, whereas [3H]CFT binding was less affected. Substitution of two serines in the eighth hydrophobic region yielded wild-type values for [3H]dopamine and [3H]MPP+ uptake and [3H]CFT binding. These results demonstrate that aspartate and serine residues lying within the first and seventh hydrophobic putative transmembrane regions are crucial for DAT function and provide identification of residues differentially important for cocaine binding and for dopamine uptake.

1-Methyl-4-phenylpyridinium↗
PubMed1992

Parkinsonism-inducing neurotoxin MPP+: uptake and toxicity in nonneuronal COS cells expressing dopamine transporter cDNA.

Expression of a cloned dopamine transporter complementary DNA in COS cells allows these primate kidney cells to accumulate the parkinsonism-inducing neurotoxin metabolite MPP+ (1-methyl-4-phenylpyridinium) avidly, and MPP+ toxicity results. By documenting that the dopamine transporter can confer MPP+ sensitivity to nonneural cells, these results highlight the key role that this transporter could play in mechanisms underlying parkinsonism.

1-Methyl-4-phenylpyridinium↗
PubMed1992

Dopamine transporter mRNA: dense expression in ventral midbrain neurons.

Oligonucleotides and a full-length cDNA encoding a functional dopamine transporter (DAT1) hybridize to a 3.7 kb mRNA that is concentrated in mRNA prepared from midbrain and absent in specimens from cerebellum or cerebral cortex. In situ hybridization reveals substantial hybridization densities overlying neurons of the substantia nigra, pars compacta, and the parabrachialis pigmentosus region of the ventral tegmental area (VTA). Neurons in the linear and paranigral VTA regions display lower levels of expression. Preliminary studies in arcuate neurons suggest modest hybridization. Different dopaminergic cell groups display different levels of DAT1 dopamine transporter expression.

Animals↗
PubMed1991

Cloning and expression of a cocaine-sensitive dopamine transporter complementary DNA.

A rat dopamine (DA) transporter complementary DNA has been isolated with combined complementary DNA homology and expression approaches. The DA transporter is a 619-amino acid protein with 12 hydrophobic putative membrane-spanning domains and homology to the norepinephrine and gamma-aminobutyric acid transporters. The expressed complementary DNA confers transport of [3H]DA in Xenopus oocytes and in COS cells. Binding of the cocaine analog [3H]CFT ([3H]2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane) to transfected COS cell membranes yields a pharmacological profile similar to that in striatal membranes.

Amino Acid Sequence↗
PubMed1991

Calcium-dependent biosynthesis of platelet-activating factor by submandibular gland cells.

Isolated dog submandibular gland cells synthesize platelet-activating factor (PAF) when stimulated with acetylcholine (ACh). This production of PAF was concentration- and time-dependent, and was inhibited by pretreatment with anticholinergic agents. PAF that had accumulated in cells through prior stimulation with ACh vanished rapidly on addition of atropine. Phenylmethanesulphonyl fluoride produced an accumulation of PAF in non-stimulated cells and greatly potentiated further ACh-induced accumulation. PAF production and [14C] arachidonic acid (AA) liberation induced by ACh were increased by higher concentrations of extracellular Ca2+, and ACh failed to stimulate PAF formation in the absence of Ca2+, although ACh still stimulated the liberation of [14C]AA without Ca2+. Both the Ca2+ ionophore ionomycin in intact cells and Ca2+ (at concentrations greater than or equal to 300 nM) in digitonin-permeabilized cells facilitated PAF formation. 1-O-Alkyl-2-lyso-sn-glycero-3-phosphocholine (lyso-PAF):acetyl-CoA acetyltransferase activity rapidly increased in cells incubated with ACh or ionomycin. These results suggest, at least, that the stimulation of a remodelling pathway is involved in the increased PAF synthesis induced by ACh. Dithiothreitol-insensitive cholinephosphotransferase activity was also activated by ACh. However, the activation of both enzymes by ACh was transient, in spite of the fact that ACh-stimulated PAF formation was continuous. This may suggest that additional mechanism(s) other than the activation of these enzymes play an important role in controlling PAF synthesis. The present study provides further evidence that the exocrine submandibular gland cells of dogs have the capacity to increase PAF turnover upon stimulation in a Ca(2+)-dependent manner and retain PAF within the cells partly associated with the membrane and partly released into the cytosol.

Acetylcholine↗
PubMed1991

Calcium dependency of adrenergic and muscarinic cholinergic stimulation of mucin release from dog submandibular gland cells.

Stimulation of muscarinic cholinergic, alpha-adrenergic and beta-adrenergic receptors elicited mucin release from dispersed dog submandibular cells. The secretory response to acetylcholine was much more pronounced than to adrenergic agonists, and largely dependent on the presence of extracellular Ca2+, but the dependency on extracellular Na+ was slight. Ionomycin also stimulated mucin release. In rat submandibular cells, neither muscarinic cholinergic agonists nor ionomycin were as effective mucosecretagogues as beta-adrenergic agonists. alpha-Adrenoceptor-mediated release was decreased by chelating extracellular Ca2+ with EGTA. The beta-adrenoceptor-mediated response was diminished by extensive exposure of cells to EGTA, due at least in part to the requirement of Ca2+ for beta-adrenoceptor stimulation of cAMP formation. 8-br-cAMP stimulated 45Ca2+ release from cells preloaded with 45Ca2+. The 8-br-cAMP-induced mucin release was eliminated in ionomycin-pretreated cells, but not inhibited by chelating extracellular Ca2+ and by the treatment of the cells with TMB-8 or in the cells loaded with BAPTA. These results suggest that not only the adrenergic system but also the muscarinic cholinergic system may participate in the regulation of mucin release in dog submandibular gland, and also provide the possibility that, in addition to a cAMP-mediated mechanism, Ca(2+)-dependent mechanisms may be involved in mucosecretion in dog submandibular acini.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Pharmacological evidence for the possible involvement of repetitive action potentials in facilitation by GABA of catecholamine secretion in bovine adrenal chromaffin cells.

1. gamma-Aminobutyric acid (GABA) evokes catecholamine (CA) secretion and enhances the stimulation-evoked CA secretion via facilitation of Ca2+ entry in a Cl(-)-dependent manner. The present study was designed to investigate further the ionic mechanism of modulation by GABA of CA secretion from adrenal medulla, using a primary culture of bovine chromaffin cells. 2. Tetrodotoxin (TTX), a voltage-sensitive Na+ channel blocker, reduced GABA-evoked CA secretion. 3. Inhibition of the sodium pump by ouabain or removal of extracellular K+ enhanced GABA-evoked CA secretion in a TTX-sensitive manner. 4. Tetraethylammonium (TEA) and cesium, which are known to block some types of K+ channels, markedly enhanced GABA-evoked CA secretion in a concentration-related fashion. TEA-induced enhancement of the GABA-evoked CA secretion was attenuated by TTX or replacement of extracellular Na+ by choline. On the other hand, ouabain accelerated the effect of TEA. 5. TEA and ouabain also enhanced GABA-induced Ca2+ influx and accumulation of cytosolic Ca2+, assessed with 45Ca2+ uptake and quin2 fluorescence. 6. Veratridine increased accumulation of cytosolic Ca2+ in a TTX-sensitive manner. GABA facilitated the veratridine-induced elevation of cytosolic Ca2+ even when the GABA-induced rise of cytosolic Ca2+ levelled off. 7. These results suggest the involvement of repetitive action potentials in modulation of GABA by Ca2+ mobilization and, as a consequence, of the CA secretion in chromaffin cells.

Action Potentials↗
PubMed1991

Enhancement of potassium ion activity in cat hippocampus during REM sleep.

During slow-wave sleep, extracellular potassium ion activity in the dorsal hippocampus of the cat was comparable to that during quiet wakefulness. During rapid eye movement (REM) sleep, it showed a gradual increase by 0.2-0.3 mM in the CA1 pyramidal layer and its close vicinity. No phasic increase was observed when REM bursts occurred. The enhanced K+ activity during REM sleep is considered to reflect the overall activity of the neurons in the pyramidal layer.

Animals↗
PubMed1990

Bis-oxonol experiment on plasma membrane potentials of bovine adrenal chromaffin cells: depolarizing stimuli and their possible interaction.

Changes of plasma membrane potential of isolated bovine adrenal chromaffin cells were monitored by fluorescent probe, bis-[1,3-diethyl-thiobarbiturate]trimethineoxonol (bis-oxonol), which responds to depolarization, resulting in increase of its fluorescence. Excess K+, gramicidin D, veratridine and ouabain all increased bis-oxonol fluorescence. Cells challenged with acetylcholine (ACh) or gamma-aminobutyric acid (GABA) produced a steady-state increase of bis-oxonol fluorescence, reflecting that averaged depolarization occurred continuously. Both effects were dependent on concentration with similar range, and mediated via nicotinic ACh receptor and GABAA receptor, respectively. Application of GABA with ACh or veratridine not only simultaneously but also pretreatedly caused an additive increment of bis-oxonol fluorescence. These results suggest that chromaffin cells in vitro reveal an additively enhanced change of plasma membrane potential in response to the combination of depolarizing stimuli.

Acetylcholine↗
PubMed1990

GABAA receptor-mediated increase of cytosolic Ca2+ in isolated bovine adrenal chromaffin cells.

We have studied the effects of GABA on cytosolic free Ca2+ concentration ([Ca2+]i) as a means of investigating the role of GABA in adrenal catecholamine (CA) secretion. It was demonstrated that GABA caused an elevation of [Ca2+]i via the GABAA receptor in a concentration-dependent manner, which was well correlated with an increase of 45Ca uptake, an increase of CA release and a depolarization of chromaffin cells assessed with bis-oxonol fluorescence. Since the GABA-induced rise of [Ca2+]i was absolutely dependent on the presence of extracellular Ca2+ and partly sensitive to nifedipine, at least one entry route for Ca2+ facilitated by GABA via a voltage-sensitive Ca2+ channel was suggested. When extracellular Cl- was lowered, GABA-induced CA release, depolarization, and rise of [Ca2+]i were all markedly enhanced. It is possible that GABA plays a modulatory role in the regulation of adrenal CA secretion as a facilitatory modulator.

Adrenal Glands↗
PubMed1990

Enhancement by GABA of the stimulation-evoked catecholamine release from cultured bovine adrenal chromaffin cells.

The possible involvement of GABAergic mechanisms in the catecholamine (CA) release from adrenal medulla was investigated in a primary culture of bovine adrenal chromaffin cells. GABA elicited CA release and enhanced acetylcholine (ACh)-, excess K(+)- and veratridine-evoked CA release. Muscimol, a selective GABAA receptor agonist, mimicked the action of GABA on CA release. On the other hand, baclofen, a GABAB receptor agonist, failed to affect basal or evoked CA release. Furthermore, bicuculline and picrotoxin blocked the enhancement by GABA of veratridine-evoked CA release without affecting basal CA release and CA release evoked by veratridine. In Ca2(+)-free medium, GABA failed to affect basal and caffeine-evoked CA release. ACh-evoked CA release was slightly reduced by bicuculline, whereas excess K(+)-evoked CA release was not, suggesting the involvement of endogenous GABA in CA release evoked by ACh. These results suggest a facilitatory modulation by GABA of basal and evoked release of CA from bovine adrenal medulla through GABAA receptor-mediated mechanisms.

Acetylcholine↗
PubMed1990

GABAergic modulation of catecholamine release from cultured bovine adrenal chromaffin cells. Evidence for the involvement of Cl(-)-dependent Ca2+ entry.

The mode by which GABA facilitates the basal and stimulation-evoked catecholamine (CA) release from cultured bovine adrenal chromaffin cells was investigated. Muscimol, a GABAA receptor agonist, facilitated 45Ca uptake in a concentration-related manner. When GABA and acetylcholine (ACh) were simultaneously applied, additive increase in 45Ca uptake was observed. Similar effect on 45Ca uptake was observed in the presence of GABA and veratridine, although 45Ca uptake induced by a rather low concentration of veratridine was more than additively enhanced by GABA. GABA-evoked CA release was also more than additively enhanced by BayK 8644 whereas there was only an additive effect on 45Ca uptake. Substitution of extracellular Cl- by sucrose ("low Cl- medium") during the stimulation with GABA enhanced GABA-evoked CA release. Substitution of extracellular Cl- for more than 1 h abolished GABA-evoked CA release and 45Ca uptake. At this time, the concentration-response curve for veratridine-evoked CA release was shifted to left and GABA no longer enhanced veratridine-evoked CA release at any concentration of veratridine. GABA-induced facilitation of 45Ca uptake in the presence of low concentration of veratridine was also inhibited by long-term treatment with low Cl- medium. These results suggest that the Cl(-)-dependent process linked to GABAA receptor acts on voltage-sensitive Ca2+ channels in chromaffin cells to elicit and modulate CA release.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Interaction between affect and cognition in word perception.

Investigated the hypothesis that the accuracy with which a briefly shown word is perceived depends on both the affective tone of the word and the activation of the corresponding memory code. To increase activation, expectation and word frequency were manipulated. Ss were exposed to a 25-ms flash of a target word. They then chose, from a word pair, the target word. In half the trials, this word pair was given before the flash to create an expectation. Consistent with the hypothesis, when the words were infrequent, accuracy in perception was lower for affective than for neutral words regardless of expectation. When the words were frequent, there was no effect of affective tone in the absence of expectation; in the presence of expectation, accuracy was higher for affective than for neutral words. The valence of the affective words had no effect. Results are interpreted in terms of attentional mechanisms implicated in conscious perception.

Adult↗
PubMed1990

Peripheral and ovarian venous concentrations of estradiol and progesterone in postmenopausal women with "non-endocrine" ovarian tumors.

Estradiol (E2) and progesterone (P4) levels in peripheral venous blood were measured in 45 postmenopausal (more than 5 years after menopause) women with ovarian neoplasms. The E2 and P4 concentrations in ovarian venous blood were also measured in 26 of these 45 patients. The steroid levels were compared with the values in 10 postmenopausal women without ovarian tumors. In peripheral venous blood, relatively high E2 concentrations were found in 24 of the 45 (53%) postmenopausal patients with ovarian tumors, and relatively high P4 concentrations were noted 15 of 45 (33%) of the patients. In ovarian venous blood, relatively high values of E2 were found in 18 of 26 (69%) of the postmenopausal patients, and relatively high values of P4 were noted in 11 of these 26 (42%). No differences in the E2 and P4 levels in peripheral and ovarian venous blood were noted between the patients with benign tumors and those with malignant tumors. These results suggest that some of the epithelial ovarian tumors in postmenopausal women have steroid-producing activity.

Estradiol↗