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Potassium stimulation

Neurotransmitter release induced by potassium-dependent depolarization is a physiologically relevant way to investigate pyrethroid effects on calcium-dependent neurotransmitter release since this process is independent of voltage-sensitive sodium channels [71]. Furthermore, potassium-stimulated calcium influx and subsequent neurotransmitter release by synaptosomes is blocked by a variety of voltage-sensitive calcium channel antagonists but not by TTX [4, 71, 72]. [Pg.62]

Mercuric chloride is thought to gain access to the intracellular compartment through Na + and Ca2 + channels in the membrane [ 100]. Sulphydryl reagents, including Hg2 +, could inhibit K +-stimulated uptake of Ca2+ into rat brain synaptosomes in vitro [101]. In muscle sarcoplasmic reticulum, Hg2+ causes inhibition of ATP-dependent Ca2 + uptake and loss of accumulated calcium [ 102,103]. However, HgCl2 has been found to inhibit ATP-dependent calcium uptake more strongly than it inhibits potassium-stimulated uptake [ 104],... [Pg.196]

Acrylonitrile shows an inhibitory effect on potassium-stimulated respiration of guinea-pig brain cortex slices at 1 mM, but little effect on the liver at the same concentration. A stronger anaesthetic action of acrylonitrile was detected in vitro on the sciatic nerve of Rana nigra maculata, compared with some other anaesthetic agents (Hashimoto Kanai, 1965). [Pg.79]

Ortiz G. G., Sanchez-Ruiz M. Y., Tan D. X., Reiter R. J., Benitez-King G., and Beas-Zarate C. (2001). Melatonin, vitamin E, and estrogen reduce damage induced by kainic acid in the hippocampus potassium-stimulated GABA release. J. Pineal Res. 31 62-67. [Pg.236]

Greber, S., Schwarzer, C. and Sperk, G. (1994). Neuropeptide Y inhibits potassium-stimulated glutamate release through Y2 receptors in rat hippocampal slices in vitro. Br. J. Pharmacol. 113(3), 737-740. [Pg.216]

Approximately six years ago vanadate was identified as a contaminant in commercially prepared (Sigma) ATP56, that inhibits the sodium- and potassium-stimulated... [Pg.149]

Thiazolidines have been reported to be a core scaffold for antiulcer compounds. La Mattina et al. have evaluated a series of 128 compounds belonging to 4-substituted-2-guanidino thiazoles (Fig. 12) against gastric hydrogen-potassium stimulated adenosine triphosphatase (H K -ATPase), a therapeutic target of anti-ulcer drugs [116]. [Pg.197]

FIGURE 3 Effects on the guanylate cyclase activator, atrial natriuretic peptide II (ANP II), on Ca +-dependent activation of phosphorylase a formation and intracellular Ca levels in potassium-stimulated (A and C) or vasopressin-stimulated (B and D) primary cultures of rat aortic VSMC. Cultures were incubated for one minute with the Ca +-activating stimulus in the absence or presence of different concentrations of ANP II. Asterisk denotes significance from 0 ANP II at P < 0.05. For details on the methodology, consult Corwell and Lincoln (1988). Reprinted with permission from the Journal of Pharmacol. Exp. Therap. and Williams and Wilkins, Co., Copyright 1988. [Pg.260]

Machiyama Y, Balazs R., Hammond B. ], Julian T, and Richer D. (1970) The metabolism of GABA and glucose in potassium stimulated brain tissue in vitro Biochem f 116, 469-482. [Pg.232]

Pearce B R., Currie D N, Beale R., and Dutton G R. (1981) Potassium-stimulated, calcium-dependent release of [ H] GABA from neuron-and gha-ennched cultures of cells dissociated from rat cerebellum Brain Res 206, 485-489... [Pg.269]

Sellstrom A and Hamberger A. (1977) Potassium-stimulated 7-aminobutyric acid release from neurons and glia Brain Res 119, 189-198... [Pg.271]

Riklis, E., Quastel, J.H. Effects of metabolic inhibitors on potassium-stimulated glucose absorption by isolated surviving guinea pig intestine. Canad. J. Biochem. 36, 363-367 (1958)... [Pg.535]

Whereas sodium participates in metabolism mainly by its cationic properties, potassium is more directly involved in metabolism. Potassium stimulates the activity of a specific enzyme— pyruvic kinase—and is required for the phosphorylation of fructose-1-phosphate to fructose-1,6-diphosphate. Similarly, potassium stimulates acetyl kinase activity. Many alterations in the bioenergetic pathways of the cell are accompanied by changes in the intracellular concentration of potassium. After insulin administration, some of the potassium of the extracellular fluid is transferred inside the cells. During oxidative phosphorylation, potassium accumulates inside the mitochondria, and dinitrophenol uncouples the ion penetration and the oxidation. [Pg.569]

R. W. Wightman In the potassium stimulation, it does not return to base line very quickly because there is lots of potassium around. In the electrical stimulation, it gets to within 90% of base line within 10 to 12 s and by 8 min it is absolutely indistinguishable from base line. If the dopamine was metabolized we would see a very small contribution to that base line change and I think that might be part of the problem. But the important fact is that it is decaying in a very nice exponential fashion, following first order kinetics out to about 15 s. [Pg.203]

Figure 18 Representative current-time traces for exocytosis from varicosities of two differentiated PC12 cells. Potassium chloride (105 mM) was ejected (at arrows) from the microinjector to perfuse the area surrounding the electrode and varicosity of interest. (A) Immediate release of dopamine (DA) following potassium stimulation, representative of 9 of the 16 cells. The second stimulation and release indicates that the varicosity is stiU responsive after initial stimulation. (B) Representative data from one of the seven cells that exhibited a delay between the time of stimulation with 105 mM potassium chloride and secretion of DA. The mean vesicle content in both immediate and delayed release is 178 zmol. The 5 pm carbon fiber electrode is held at a potential of 0.65 V vs. SSCE for aU measurements. The inset is an example of a typical current transient observed at a varicosity displayed on an expanded time scale. The release time (3 ms rise-time of the current spike) is similar to that observed at an undifferentiated cell (Reproduced from Brain Res. with permission [3].)... Figure 18 Representative current-time traces for exocytosis from varicosities of two differentiated PC12 cells. Potassium chloride (105 mM) was ejected (at arrows) from the microinjector to perfuse the area surrounding the electrode and varicosity of interest. (A) Immediate release of dopamine (DA) following potassium stimulation, representative of 9 of the 16 cells. The second stimulation and release indicates that the varicosity is stiU responsive after initial stimulation. (B) Representative data from one of the seven cells that exhibited a delay between the time of stimulation with 105 mM potassium chloride and secretion of DA. The mean vesicle content in both immediate and delayed release is 178 zmol. The 5 pm carbon fiber electrode is held at a potential of 0.65 V vs. SSCE for aU measurements. The inset is an example of a typical current transient observed at a varicosity displayed on an expanded time scale. The release time (3 ms rise-time of the current spike) is similar to that observed at an undifferentiated cell (Reproduced from Brain Res. with permission [3].)...
Figure 19 Distribution of vesicle content for potassium-stimulated release at varicosities plotted as the cubed root of catecholamine released. Plots of the percent of total events observed in the first 40 s following initiation of release vs. the cubed root of the amount of catecholamine released upon elevated potassium stimulation for (A) 17 undifferentiated PC12 cells (475 total release events) and (B) 16 differentiated PC 12 cells (156 total release events). (Reproduced from Brain Res. with permission [3].)... Figure 19 Distribution of vesicle content for potassium-stimulated release at varicosities plotted as the cubed root of catecholamine released. Plots of the percent of total events observed in the first 40 s following initiation of release vs. the cubed root of the amount of catecholamine released upon elevated potassium stimulation for (A) 17 undifferentiated PC12 cells (475 total release events) and (B) 16 differentiated PC 12 cells (156 total release events). (Reproduced from Brain Res. with permission [3].)...
A second phase of the work made use of a radioligand assay for N-type channel binding in the chick brain. Using radiolabelled (o-conotoxin GVIA ((d-CTX), a peptide calcium channel antagonis, we confirmed the diversity of (o-agatoxin in funnel web spider venom and described a new class of toxins (Type III) which have broad specificity for vertebrate high threshold calcium channels. Subsequently, we used potassium stimulated synaptosomal calcium flux to discover toxins that block P-type calcium channels in the mammalian bndn. [Pg.252]

Figure 5. Block of potassium-stimulated Ca entry into rat brain synaptosomes by two (o-agatoxins, co-Aga-IVA and o)-Aga-IVB. These toxins selectively antagonize P-type csdcium channels in the mammalian brain. This flux assay was used to screen for this type of biological activity in the crude venom. Figure 5. Block of potassium-stimulated Ca entry into rat brain synaptosomes by two (o-agatoxins, co-Aga-IVA and o)-Aga-IVB. These toxins selectively antagonize P-type csdcium channels in the mammalian brain. This flux assay was used to screen for this type of biological activity in the crude venom.
Travis, R. L. and Booz, M. L., 1979, Partial characterization of a potassium stimulated adenosine triphosphatase from plasma membrane of meristematic and mature soybean root tissue. Plant Physiol., 63 573. [Pg.208]

FIGURE 14.11 A 1 s time period of an exocytotic response of a PC12 cell after potassium stimulation showing simultaneous detection of concurrent events at different locations on the same cell. Red arrows indicate these events. (From Zhang, B. et al.. Anal Chem., 80, 1394, 2008. With permission.)... [Pg.524]


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See also in sourсe #XX -- [ Pg.203 ]




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