1991
DOI: 10.1111/j.1471-4159.1991.tb08280.x
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Ca2+‐Independent, Ca2+‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Abstract: Synaptoneurosomes obtained from the cortex of rat brain prelabeled with [14C]arachidonic acid [( 14C]AA) were used as a source of substrate and enzyme in studies on the regulation of AA release. A significant amount of AA is liberated in the presence of 2 mM EGTA, independently of Ca2+, primarily from phosphatidic acid and polyphosphoinositides (poly-PI). Quinacrine, an inhibitor of phospholipase A2 (PLA2), suppressed AA release by about 60% and neomycin, a putative inhibitor of phospholipase C (PLC), reduced … Show more

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Cited by 31 publications
(5 citation statements)
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“…It is conceivable, however, that the intense hypercapnic-acidic stimulus and high K+ activate additional intraglomic structures to produce PGE2. The notion that chemoreceptor cells are the origin of stimulus-induced PGE2 is also strengthened by the fact that all the stimuli tested in the present study increase [Ca21]i in chemoreceptor cells (Biscoe & Duchen, 1990;Obeso, Rocher, Fidone & Gonzalez, 1992;Gonzalez et al 1992;Sato, Yoshizaki & Koyamo, 1993), this ion being an activator of phospholipases (Irvine, 1982;Berridge, 1987;Strosznajder & Samochocki, 1991), the enzymes that provide arachidonate to cyclo-oxygenase. Taking this into account, it seems plausible that the increase in PGE2 synthesis that takes place in the CB during stimulation is, at least in part, secondary to stimulus-induced elevation of [Ca2+]i in chemoreceptor cells, although other possibilities exist.…”
Section: Discussionsupporting
confidence: 53%
See 1 more Smart Citation
“…It is conceivable, however, that the intense hypercapnic-acidic stimulus and high K+ activate additional intraglomic structures to produce PGE2. The notion that chemoreceptor cells are the origin of stimulus-induced PGE2 is also strengthened by the fact that all the stimuli tested in the present study increase [Ca21]i in chemoreceptor cells (Biscoe & Duchen, 1990;Obeso, Rocher, Fidone & Gonzalez, 1992;Gonzalez et al 1992;Sato, Yoshizaki & Koyamo, 1993), this ion being an activator of phospholipases (Irvine, 1982;Berridge, 1987;Strosznajder & Samochocki, 1991), the enzymes that provide arachidonate to cyclo-oxygenase. Taking this into account, it seems plausible that the increase in PGE2 synthesis that takes place in the CB during stimulation is, at least in part, secondary to stimulus-induced elevation of [Ca2+]i in chemoreceptor cells, although other possibilities exist.…”
Section: Discussionsupporting
confidence: 53%
“…[Ca21]i in chemoreceptor cells (Biscoe & Duchen, 1990;Obeso, Rocher, Fidone & Gonzalez, 1992;Gonzalez et al 1992;Sato, Yoshizaki & Koyamo, 1993), this ion being an activator of phospholipases (Irvine, 1982;Berridge, 1987;Strosznajder & Samochocki, 1991), the enzymes that provide arachidonate to cyclo-oxygenase. Taking this into account, it seems plausible that the increase in PGE2 synthesis that takes place in the CB during stimulation is, at least in part, secondary to stimulus-induced elevation of [Ca2+]i in chemoreceptor cells, although other possibilities exist.…”
Section: Discussionmentioning
confidence: 99%
“…This interpretation is supported by several observations: 1) As shown on striatal neuronal cultures, in the absence of magnesium NMDA stimulates in a concentration-dependent manner the release of arachidonic acid (Dumuis et al, 1988). Similarly, by acting through M 1 muscarinic receptors ACh also stimulates the release of arachidonic acid (Strosznajder and Samochocki, 1991;Tencé et al, 1994) and, in addition, important synergistic effects on arachidonic acid formation are observed under the combined application of NMDA and ACh (or carbachol) (Tencé et al, 1995). 2) As shown in our laboratory, in the rat striatum arachidonic acid inhibits the reuptake of GABA and induced a marked facilitation of its release process through a mechanism which is calcium-dependent and partially results from the activation of a protein kinase C. In addition, the latter effects are not reproduced by other fatty acids and persist following blockade of the main metabolic pathways of arachidonic acid (Chéramy et al, 1996).…”
Section: Suppression By Mepacrine and Bovine Serum Albumin Of The Gabmentioning
confidence: 61%
“…The pellet was resuspended in 5 mL of fresh buffer and gently filtered through three layers of nylon mesh (pore size, 100 µm) using a plastic syringe (20-mL capacity), and the resulting filtrate was centrifuged at 1100g for 15 min to obtain a synaptoneurosomal pellet. This fraction was examined by electron microscopy as described previously by Strosznajder and Samochocki (1991).…”
Section: Preparation Of Synaptoneurosomesmentioning
confidence: 99%