Arachidonic acid evokes inositol phospholipid hydrolysis in astrocytes

Murphy, Seán; Welk, Greg

doi:10.1016/0014-5793(89)81788-0

Cited by 23 publications

(7 citation statements)

References 16 publications

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“…Arachidonic acid could mediate the effect of 2-chloroadenosine, because the unsaturated fatty acid has been shown to open K+ channels on atrial membranes (Kim et al, 1989), thus reproducing the effect of the nucleoside on striatal neurons (Trussel and Jackson, 1985). By increasing the driving force for Ca", this expected hyperpolarization could, in turn, improve the influx of Ca2+ stimulated by [~-Pro']-substance P. In addition, arachidonic acid could further stimulate the activity of phospholipase C, as already shown in cultured astrocytes (Murphy and Welk, 1989). These two mechanisms could explain the sustained action of the unsaturated fatty acid which appears to mediate the effects of the nucleoside.…”

Section: Discussionmentioning

confidence: 62%

Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Delumeau

Petitet

Cordier

et al. 1991

Journal of Neurochemistry

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The effects on cytosolic Ca2+ concentration of 2-chloroadenosine and [L-Pro9]-substance P, a selective agonist of NK1 receptors, were investigated on astrocytes from embryonic mice in primary culture. Cells responded to [L-Pro9]-substance P with a transitory increase in cytosolic Ca2+ which was of shorter duration when external Ca2+ was removed. A transient response to 2-chloroadenosine alone occurred. When simultaneously applied, [L-Pro9]-substance P and 2-chloroadenosine evoked a prolonged elevation of cytosolic Ca2+ (up to 30 min). This phenomenon was dependent on the presence of extracellular Ca2+, but insensitive to dihydropyridines, La3+, and Co2+, excluding the implication of voltage-operated Ca2+ channels. Arachidonic acid also induced a sustained elevation of cytosolic Ca2+, but did not increase further the response evoked by [L-Pro9]-substance P and 2-chloroadenosine. The activation of protein kinase C by a diacylglycerol analogue mimicked the effect of [L-Pro9]-substance P in potentiating the 2-chloroadenosine-evoked response. Like 2-chloroadenosine, pinacidil, which hyperpolarizes the cells by opening K+ channels, prolonged the elevation of cytosolic Ca2+ concentration induced by [L-Pro9]-substance P. Conversely, depolarization with 50 mM KCl canceled the effects of either pinacidil or 2-chloroadenosine applied with [L-Pro9]-substance P. Pertussis toxin pretreatment suppressed all the effects induced by 2-chloroadenosine.

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Section: Discussionmentioning

confidence: 62%

Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Delumeau

Petitet

Cordier

et al. 1991

Journal of Neurochemistry

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“…ARA had an inhibitory effect on PtdIns-1,4-P2/PtdIns-1,4,5-P3 metabolism under condition of cycle activation in submandibular acinar cells [44]. In contrast, it stimulated the accumulation of inositol mono-bi-and tri-phosphate, but not inositol phosphoglycerides in astrocytes [45]. Also, it is reported that ARA PtdCho suppressed Akt membrane translocation but left the concentration of the anchor lipid phosphatidylinositol-3,4,5-trisphosphate unchanged in fibroblasts [46].…”

Section: Discussionmentioning

confidence: 87%

Phosphorylation of protein kinase B, the key enzyme in insulin-signaling cascade, is enhanced in linoleic and arachidonic acid–treated HT29 and HepG2 cells

2019

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“…By increasing the driving force this expected hyperpolarization should in turn improve Ca2+ influx through putative Ca2+ or non-specific cationic channels, when phospholipase C is stimulated by the al-agonist, methoxamine. AA could also exert a positive feedback on the regulation of cytosolic Ca2+ concentration by activating further phospholipase C, as already shown on cultured astrocytes (Murphy and Welk, 1989) and according to the dramatic shortening of the response latency. The dual mechanism of the unsaturated fatty acid could explain its sustained action (Fig.…”

Section: Discussionmentioning

confidence: 90%

Synergistic Regulation of Cytosolic Ca²⁺ Concentration by Adenosine and α1‐Adrenergic Agonists in Mouse Striatal Astrocytes

Delumeau

Tencé

Marin

et al. 1991

Eur J of Neuroscience

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Adenosine has a broad array of actions on neurons but astrocytes also possess adenosine receptors. We have previously shown that adenosine, by acting on astrocytes in the striatum, can modulate neuronal responses mediated by receptors coupled to phospholipase C through an astrocyto - neuronal interaction. In addition, adenosine was found to potentiate the alpha1-adrenergic production of inositol phosphates in astrocytes. The mechanism involved in this potentiation was further investigated by examining the effects of adenosine and alpha1-adrenergic receptor agonists on cytosolic Ca2+ in cultured striatal astrocytes from the embryonic mouse in primary culture. When used alone, methoxamine, a selective agonist of alpha-adrenergic receptors or 2-chloroadenosine, a stable analogue of adenosine, induced a transitory increase in cytosolic Ca2+, but their combined addition led to a sustained increase in cytosolic Ca2+, which seems to be due to a Ca2+ influx, because it was not observed in the absence of external Ca2+. Voltage independent Ca2+ channels contribute to this process and different blockers of voltage-operated calcium channels, such as dihydropyridines, phenylalkylamines, La3+ or Co2+ were ineffective in suppressing the sustained cytosolic Ca2+ elevation. Three observations suggest the implication of arachidonic acid in the observed potentiation: (i) arachidonic acid induced a sustained elevation of cytosolic Ca2+ similar to that evoked by the coapplication of methoxamine and 2-chloroadenosine; (ii) the addition of arachidonic acid during the calcic plateau produced by the combined application of the agonists did not increase further cytosolic Ca2+ levels; (iii) in the presence of methoxamine, 2-chloroadenosine induced a release of arachidonic acid. The stimulation of phospholipase C and the resulting activation of protein kinase C induced by methoxamine seem to be required for the potentiating effect of 2-chloroadenosine on cytosolic Ca2+. In fact, the direct activation of protein kinase C by an exogenous diacylglycerol analogue mimicked the effect of methoxamine because, in this condition, 2-chloroadenosine alone evoked a sustained elevation of cytosolic Ca2+. Therefore, methoxamine, through the successive activation of phospholipase C and protein kinase C, could allow a lipase, probably phospholipase A2, to be stimulated by 2-chloroadenosine. Arachidonic acid has already been shown to trigger the opening of K+ channels and the formation of inositol phosphates in other cell types. Therefore, in striatal astrocytes, 2-chloroadenosine, through an arachidonic acid-mediated hyperpolarization, could increase the Ca2+ driving force and thus improve Ca2+ influx through inositol phosphate-gated channels. This hypothesis is further supported by the suppressing effect of a 50 mM KCI-induced depolarization on the long lasting elevation of cytosolic Ca2+ seen in the combined presence of 2-chloroadenosine and methoxamine.

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Arachidonic acid evokes inositol phospholipid hydrolysis in astrocytes

Cited by 23 publications

References 16 publications

Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Phosphorylation of protein kinase B, the key enzyme in insulin-signaling cascade, is enhanced in linoleic and arachidonic acid–treated HT29 and HepG2 cells

Synergistic Regulation of Cytosolic Ca²⁺ Concentration by Adenosine and α1‐Adrenergic Agonists in Mouse Striatal Astrocytes

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Arachidonic acid evokes inositol phospholipid hydrolysis in astrocytes

Cited by 23 publications

References 16 publications

Synergistic Regulation of Cytosolic Ca2+ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Synergistic Regulation of Cytosolic Ca2+ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Phosphorylation of protein kinase B, the key enzyme in insulin-signaling cascade, is enhanced in linoleic and arachidonic acid–treated HT29 and HepG2 cells

Synergistic Regulation of Cytosolic Ca2+ Concentration by Adenosine and α1‐Adrenergic Agonists in Mouse Striatal Astrocytes

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Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Synergistic Regulation of Cytosolic Ca²⁺ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists

Synergistic Regulation of Cytosolic Ca²⁺ Concentration by Adenosine and α1‐Adrenergic Agonists in Mouse Striatal Astrocytes