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Query: CAS:7440-70-2 (calcium)
 333,191 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of alpha-latrotoxin on cerebral cortex slices was studied by both biochemical and morphological methods. This toxin greatly stimulates the release of preloaded gamma-amino[3H]butyric acid from cortex slices. The response increases linearly with dose. The release is not dependent on the presence of extracellular Ca2+, and therefore it is not mediated by the release of other transmitters from other types of neurons. In contrast, no significant increase in the release of a nontransmitter substance alpha-amino[14C]isobutyric acid is observed. Since previously we have shown that alpha-latrotoxin stimulated the release of acetylcholine and norepinephrine from cortex slices, it appears that the toxin probably selectively releases all neurotransmitters. The toxin also profoundly depletes the synaptic vesicle population in boutons in the cortex slices. The results suggest that the release of neurotransmitter and the depletion of synaptic vesicle in boutons are manifestations of a single action of the toxin. Therefore, alpha-latrotoxin can be used as a good tool for the identification of neurotransmitters and in studies on the mechanism of neurotransmitter release.
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PMID:Release of neurotransmitters and depletion of synaptic vesicles in cerebral cortex slices by alpha-latrotoxin from black widow spider venom. 27 18

1. The influx of [3H]gamma-aminobutyric acid ([3H]GABA) into isolated rat superior cervical ganglia has been measured by radioassay, supplemented by autoradiography. Ganglia were incubated in oxygenated Krebs solution at 25 degrees C, containing 10 microM-amino-oxyacetic acid. Under these conditions more than 95% of accumulated tritium was unmetabolized [3H]GABA. 2. Ganglionic radioactivity increased linearly with incubation time, to yield an intracellular fluid/extracellular fluid concentration ratio (Ci/Co) of about 200 after 6 hr in 0.5 microM-external [3H]GABA. 3. Uptake showed saturation with an apparent transport constant (KT) of 6.8 microM and maximum influx velocity (Jmaxi) of 7 mumole 1. cell fluid-1- min-1. 4. The influx rate at Co = 0.5 microM was unaltered by raising intracellular GABA from 0.2 to 1 mM. 5. Influx velocity increased with temperature (5--35 degrees C) in a monotonic manner with an apparent activation energy of 14 kcal mole-1. 6. Concentrative uptake was depressed by reducing external [Na+] with ouabain, by raising [K+]o above 20 mM, or by removing external Cl-. Uptake was not particularly sensitive to Ca2+ or Mg2+ ions. 7. Utake of [3H]GABA (0.5 microM) was inhibited by beta-guanidinopropionic acid (apparent KI, 28 microM), beta-alanine (KI, 55 microM), gamma-amino-beta-hydroxybutyric acid (KI, 220 microM), beta-amino-n-butyric acid (KI, 708 microM), 3-aminopropanesulphonic acid (KI, 832 microM) and taurine (KI greater than 1 mM). Uptake was not depressed by 1 mM-glycine, alpha-alanine, leucine, serine, methionine or alpha-amino-iso-butyric acid. 8. Radioactively labelled methionine, leucine, glycine, serine, beta-alanine and taurine (concentrations less than or equal to 5 microM) were also taken up by ganglia. Of these, only uptake of beta-alanine and taurine were significantly depressed by 1 mM-GABA. 9. Autoradiographs confirmed that [3H]GABA and [3H] beta-alanine were taken up predominantly into extraneuronal sites (presumed to be neuroglial cells). Methionine, leucine, glycine and serine showed preferential accumulation in neurones. Neuronal uptake of leucine was not prevented by inhibiting protein synthesis. 10. Calculations of net fluxes from unidirectional tracer fluxes suggest that the sympathetic glial cells are capable of promoting net uptake of GABA at external concentrations above 1 microM.
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PMID:[3H]gamma-Aminobutyric acid uptake into neuroglial cells of rat superior cervical sympathetic ganglia. 50 28

1. A carboxylesterase (carboxylic-ester hydrolase, EC 3.1.1.1) from human brain extract was prepared to purity using DEAE-cellulose, Sephadex G-200, and fractionation with (NH4)2SO4. The yield was about 20%. 2. Esters of butyric acid were split faster than esters of acetic, propionic and valeric acid, and the enzyme is tentatively designated as a butyrylesterase. Thiocholine esters were split at low rates. 3. The molecular weight was estimated as 340 000 using gel chromatography on Sephadex G-200. In isoelectric focussing the enzyme was resolved into several peaks (pI 4.0--4.7). The low isoelectric point does not seem to be due to terminal sialic acid residues. 4. The enzyme was irreversibly inhibited by diethyl-p-nitrophenyl phosphate (ki = 206 mol-1 - 1 - s-1) and by diisopropylfluorophosphate. The carboxylesterase inhibitor bis-p-nitrophenyl phosphate and eserine did not inhibit the enzyme. 5. The enzyme was progressively inhibited by p-hydroxy-mercuribenzoate, and reactivated by dithiothreitol and 2-mercaptoethanol. N-Ethylmaleimide inactivated the enzyme very slowly, whereas iodoacetate and iodoacetamide were without effect. 6. Ca2+, Mg2+, and Zn2+ or EDTA did not influence the enzyme activity.
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PMID:Carboxylesterases of human brain extract. Purification and properties of a butyrylesterase. 85 94

A peripheral nervous system cell line RT4-B, established by Imada and Sueoka (Dev. Biol., 66:97-108, 1978), was shown to respond to serotonin [5-hydroxytryptamine (5-HT)] and catecholamines. 5-HT induced a small and transient increase in cytosolic free Ca2+ concentration ([Ca2+]i) in the RT4-B cells. The increase was effectively blocked by 5-HT2 receptor antagonists (spiperone, ritanserin and mianserin), but not by a 5-HT3 receptor antagonist (MDL72222), or a alpha 1-adrenergic receptor antagonist (prazosin), indicating that RT4-B cells express 5-HT2 receptors. On the other hand, catecholamines increased cyclic AMP production by RT4-B. The order of potency for stimulating cyclic AMP synthesis was isoproterenol greater than epinephrine much greater than norepinephrine much greater than dopamine, and the stimulation was effectively inhibited by the nonselective beta-adrenergic receptor antagonist propranolol, but not by the beta 1-adrenergic receptor antagonist atenolol, suggesting that RT4-B cells express beta 2-adrenergic receptors. The differentiating agent N6,2'-O-dibutyryladenosine 3',5'-monophosphate (dibutyryl-cAMP) enhanced the 5-HT-induced [Ca2+]i increase, but not the catecholamine-induced cyclic AMP production. The increase in the 5-HT response paralleled the increase in the density of 5-HT2 receptors. n-Butyric acid (2 mM) and 8-bromoadenosine 3',5'-monophosphate (1 mM) also increased the 5-HT response, and the sum of these increases was nearly equal to that induced by dibutyryl-cAMP. These results indicate that RT4-B is a novel model cell line for the study of 5-HT2 and beta 2-adrenergic receptors and their second messenger responses and for the analysis of the mechanisms how 5-HT2 receptor gene expression is controlled.
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PMID:Dibutyryl-cAMP increases functions of 5-hydroxytryptamine2 receptors, but not of beta 2-adrenergic receptors, in a clonal cell line of rat neurotumor RT4. 130 26

The results reported here indicate that the short-chain carboxylic acids acetate and propionate stimulate cytoplasmic calcium mobilization in human polymorphonuclear leukocytes, while butyrate and lactate do not. Together with the results of previous work, this indicates that there are at least three classes of short-chain carboxylic acids: those which can alter only cytoplasmic pH (e.g., lactic acid), those which can alter cytoplasmic pH and actin (e.g., butyric acid), and those which can alter cytoplasmic pH, actin, and calcium (e.g., acetate and propionate).
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PMID:Alteration of cytoplasmic Ca2+ in resting and stimulated human neutrophils by short-chain carboxylic acids at neutral pH. 145 65

In acinar cells freshly dispersed from rat parotid glands, the effects of ammonium chloride (NH4Cl) on membrane currents were studied using the whole-cell clamp method. When membrane currents were recorded with command pulses to 0 mV, applied at 2-s intervals from a holding potential of -70 mV, NH4Cl (5-20 mM) transiently decreased outward currents and then slowly increased both outward and inward currents. After reaching a peak in about 40-50 s, both outward and inward currents gradually decreased in the presence of NH4Cl and, on its wash-out, the currents returned to the control level. Butyrate (5-20 mM) had little effect on the resting membrane currents, but markedly inhibited the response to NH4Cl. Tetraethylammonium (5 mM) strongly reduced both the resting and NH4Cl-induced outward currents, whereas it slightly potentiated the NH4Cl-induced inward current without affecting the membrane current at the holding potential. Without ATP in the patch pipettes, carbachol-induced membrane currents were relatively resistant to Ca2+ removal from the external medium, but NH4Cl-induced currents were quickly abolished in the absence of Ca2+. We conclude that intracellular alkalinization with NH4Cl increases Ca2+ influx and activates Ca(2+)-dependent outward K+ and inward Cl- currents.
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PMID:Effects of ammonium chloride on membrane currents of acinar cells dispersed from the rat parotid gland. 159 85

N-Methyl-D-aspartate (NMDA) or aspartate (Asp) increased the cytosolic free calcium concentration ([Ca]in) in some populations of Purkinje cells dissociated from immature rat cerebellum. The NMDA- and Asp-induced rise in [Ca]in was affected only a little by adding glycine or NMDA antagonists, but was reduced either by adding Mg2+, Gallopamil hydrochloride (D-600) and gamma-amino-butyric acid, or by removing external Na+. The results suggest that stimulation of the NMDA-sensitive receptors transiently expressed on immature Purkinje cell soma results in a rise in [Ca]in through the activation of voltage-dependent Ca2+ channels.
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PMID:N-methyl-D-aspartate and aspartate raise the cytosolic free calcium concentration by acting upon receptors transiently expressed on immature cerebellar Purkinje cells. 168 8

Rats were fed high fat (231 g/kg diet), low calcium (1.3 g/kg diet), low cellulose (20 g/kg diet) diets in which carbohydrates were represented by sucrose or starch (460 g/kg diet). A subgroup of animals was treated with 1,2-dimethylhydrazine (DMH) twice, 4 and 8 d before the beginning of the dietary treatments. Animals fed the starch diet, compared with those fed the sucrose diet, had higher concentrations of cecal and fecal short-chain fatty acids and a significantly lower acetic acid:butyric acid ratio in the cecal contents at d 105. Ratios were 14.7 +/- 1.7 and 6.8 +/- 0.4 for rats fed the sucrose and starch diets, respectively (P less than 0.01). Cecal pH was significantly lower in animals fed the starch diet for 105 d. At d 105, rectal proliferation was lower in rats fed the starch diet (labeled cells/crypt were 7.89 +/- 0.56 and 3.57 +/- 0.40 for rats fed the sucrose and starch diets, respectively, P less than 0.01); at d 30 the effect of starch on proliferation was evident in controls but not in DMH-treated rats. Rectal proliferation data were negatively correlated with the concentration and percentage of butyric acid and positively correlated with the percentage of acetic acid, the acetic acid:butyric acid ratio and cecal pH. These results suggest that low rectal proliferation in animals fed a high fat, high starch diet might be associated with a lower relative concentration of butyric acid in the cecal contents.
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PMID:Profile of short-chain fatty acids and rectal proliferation in rats fed sucrose or cornstarch diets. 173 66

The release of preaccumulated gamma-amino[3H]butyric acid ([3H]GABA) from putative GABAergic amacrine cells was studied in neuronal monolayer cultures made from embryonic chick retina. Release was specifically stimulated by excitatory amino acid agonists. N-Methyl-D-aspartate (NMDA; EC50, 19.1 +/- 5.0 microM), kainic acid (EC50, 15.6 +/- 2.3 microM), and the presumptive endogenous ligand glutamate (EC50, 3.6 +/- 0.5 microM) showed the same efficacy. Quisqualic acid, although the most potent agonist (EC50, 0.56 +/- 0.12 microM), was only half as efficacious. The time course of [3H]GABA release and autoradiographic visualization of responsive GABA-accumulating cells suggest that approximately 50% of the [3H]GABA-accumulating cells possess no or very low responsiveness to quisqualic acid. Depolarization (56 mM KCl)-induced release was fivefold lower than the maximal effect elicited by excitatory amino acids. Release of [3H]GABA and of endogenous GABA was entirely independent of extracellular Ca2+ but was completely abolished after replacement of Na+ by choline or Li+. The effects of NMDA and low concentrations of glutamate (up to 10 microM) were blocked by 2-amino-5-phosphonovaleric acid, by MK 801, and (in a voltage-dependent manner) by Mg2+. The reduction of NMDA responses by kynurenic acid was reversed by D-serine, and quisqualic acid competitively inhibited kainic acid-evoked release. Our results show that the cultured [3H]GABA-accumulating neurons, which probably represent the in vitro counterparts of GABAergic amacrine cells, express at least two types of excitatory amino acid receptors (of the NMDA and non-NMDA type), both of which can mediate a Ca2(+)-independent but Na2(+)-dependent release of GABA.
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PMID:Release of gamma-amino[3H]butyric acid from cultured amacrine-like neurons mediated by different excitatory amino acid receptors. 184 90

This study was conducted to study digestion in rats of a diet containing soybean fiber (chiefly hemicellulose). The animals were first fed a fiber-free high starch diet for 7 d before receiving a 30% soybean fiber diet. There was a progressive change in the cecal pool of volatile fatty acids (VFA), up to approximately 1000 mumol, due to the enlargement of the cecum in conjunction with the rise of the VFA concentration, and the decrease in the cecal pH to 6. In rats fed the soybean fiber diet, the cecal concentrations of acetate and propionate increased with propionate reaching a very high value (approximately 50 mmol/L) after 22 d of dietary treatment. Butyrate concentrations first increased, then declined to about 10 mmol/L. Absorption of VFA was enhanced fivefold between d 2 and d 21 and was then 10-fold higher than in rats fed the fiber-free diet. The transfer of blood urea to the cecum increased in parallel with the enlargement of the cecum and there was a large rise of ammonia absorption after 8 d. There was a rapid increase in the cecal pool of phosphorus, whereas the cecal pools of calcium and magnesium significantly increased only after 8 d. The cecal absorption of calcium and magnesium increased very early, even when the cecal pool of these cations was not enhanced. The soybean fiber diet also elicited a strong induction of ornithine decarboxylase (ODC) in cecal mucosa, which was attenuated after 21 d of dietary treatment. Thymidine kinase was smaller than for ODC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soybean fiber on cecal digestion in rats previously adapted to a fiber-free diet. 185 Apr 56


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