Accumulations of cyclic AMP and inositol phosphates in guinea pig cerebral cortical synaptoneurosomes: enhancement by agents acting at sodium channels

Hollingsworth, Elizabeth B.; Sears, Edward B.; Cruz, R.A. de la; Gusovsky, Fabián; Daly, John W.

doi:10.1016/0304-4165(86)90129-7

Cited by 17 publications

(6 citation statements)

References 23 publications

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“…In accordance with other studies the use of filtered versus unfiltered synaptoneurosomal preparations gave comparable results (Hollingsworth et al, 1986;Gusovsky and Daly, 1988). The unfiltered preparation of synaptoneurosomes was used in our studies.…”

Section: Synaptoneurosome-enriched Preparation From Rat Brain Cortexsupporting

confidence: 91%

Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Strosznajder

Samochocki

1991

Journal of Neurochemistry

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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 AA release by about 30%. An additive effect was exhibited when both inhibitors were given together. Ca2+ activated AA release. The level of Ca2+ present in the synaptoneurosomal preparation (endogenous level) and 5 microM CaCl2 enhance AA liberation by approximately 25%, whereas 2 mM CaCl2 resulted in a 50% increase in AA release relative to EGTA. The source for Ca(2+)-dependent AA release is predominantly phosphatidylinositol (PI); however, a small pool may also be liberated from neutral lipids. Carbachol, an agonist of the cholinergic receptor, stimulated Ca(2+)-dependent AA release by about 17%. Bradykinin enhanced the effect of carbachol by about 10-15%. This agonist-mediated AA release occurs specifically from phosphoinositides (PI + poly-PI). Quinacrine almost completely suppresses calcium-and carbachol-mediated AA release. Neomycin inhibits this process by about 30% and totally suppresses the effect of bradykinin. Our results indicate that both phospholipases PLA2 and PLC with subsequent action of DAG lipase are responsible for Ca(2+)-independent AA release. Ca(2+)-dependent and carbachol-mediated AA liberation occurs mainly as the result of PLA2 action. A small pool of AA is probably also released by PLC, which seems to be exclusively responsible for the effect of bradykinin.

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Section: Synaptoneurosome-enriched Preparation From Rat Brain Cortexsupporting

confidence: 91%

Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Strosznajder

Samochocki

1991

Journal of Neurochemistry

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“…Even if all agents known to produce an overall membrane depolarization via Na+ influx, and in particular the Na+ ionophore monensin, stimulate the metabolism of Ips (Gusovsky et al, , 1987Habermann and Laux, 1986;Hollingsworth et al, 1986;Guiramand et al, 19898, 1991), the involvement of Na+ influx as a common step in the mechanism of activation of the phosphoinositide breakdown by Glu and depolarizing agents is unlikely. Indeed, the replacement of external Na' by various compounds provokes a depolarization of the synaptoneurosomal membrane, associated with an increase in accumulation of IPS .…”

Section: The Putative Common Step In the Action Of Glu And Depolarizimentioning

confidence: 99%

A Specific Transduction Mechanism for the Glutamate Action on Phosphoinositide Metabolism via the Quisqualate Metabotropic Receptor in Rat Brain Synaptoneurosomes: II. Calcium Dependency, Cadmium Inhibition

Guiramand¹,

Vignes²,

Récasens³

1991

Journal of Neurochemistry

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In this article, we demonstrate that an increase in intracellular Ca2+ concentration may represent a specific common step(s) in the mechanism(s) of action of glutamate (Glu) and depolarizing agents on formation of inositol phosphates (IPs) in 8-day-old rat forebrain synaptoneurosomes. In fact, A23187, a Ca2+ ionophore, induces a dose-dependent accumulation of IPs, which is not additive with that evoked by Glu and K+ but is slightly synergistic with that induced by carbachol. In addition, Glu and K+ augment the intracellular Ca2+ concentration in synaptoneurosome preparations as measured by the fura-2 assay. The absence of external Ca2+ decreases basal and Glu-, and K(+)-stimulated formation of IPs. Cd2+ (100 microM) fully inhibits both Glu- and K(+)-evoked formation of IPs without affecting the carbachol-elicited response of IPs. Zn2+ inhibits Glu- and K(+)-stimulated accumulation of IPs (IC50 approximately 0.4 mM) but with a lower affinity than Cd2+ (IC50 approximately 0.035 mM). The organic Ca2+ channel blockers verapamil (10 microM), nifedipine (10 microM), omega-conotoxin (2 microM), and amiloride (10 microM) as well as the inorganic blockers Co2+ (100 microM) and La3+ (100 microM) block neither Glu- nor K(+)-evoked formation of IPs, a result suggesting that the opening of the L-, T-, N-, or P-type Ca2+ channels does not participate in these responses. All these data suggest that an increase in intracellular Ca2+ concentration resulting from an influx of Ca2+, sensitive to Cd2+ but not to other classical Ca2+ antagonists, may play a key role in the transduction mechanism activated by Glu or depolarizing agents.

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“…It is now generally accepted that several cell-surface receptors are linked to phosphoinositidase C and that products of polyphosphoinositide hydrolysis are important intracellular messengers (for review, see Berridge & Irvine, 1989). In addition to the well-documented studies of receptor-mediated phosphoinositide breakdown, it is apparent that depolarization induced by elevated extracellular K+ or veratrine can also stimulate phosphoinositide hydrolysis in several tissues, particularly those of a neuronal nature (Kendall & Nahorski, 1984Bone & Michell, 1985;Baird & Nahorski, 1986, 1989, 1990Court et al, 1986;Eva & Costa, 1986;Hollingsworth et al, 1986;Gusovsky et al, 1986;Habermann & Laux, 1986;Gurwitz & Sokolovsky, 1987;Audigier et al, 1988;Sasaguri & Watson, 1988;McDonough et al, 1988). In several of these studies, indirect effects of depolarization can be eliminated and responses can be shown to be secondary to Ca2l entry via voltage-sensitive channels.…”

Section: Introductionmentioning

confidence: 99%

Differences between muscarinic-receptor- and Ca2+-induced inositol polyphosphate isomer accumulation in rat cerebral-cortex slices

Baird

Nahorski

1990

Biochemical Journal

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Muscarinic-receptor stimulation or depolarization by elevated K+ leads to increased accumulation of [3H]Ins(1,4,5)P3, [3H]Ins(1,3,4,5)P4 and several degradation products of these polyphosphates separated by h.p.l.c. On the other hand, agents such as ionomycin and maitotoxin, which increase intracellular Ca2+ directly, produce a small accumulation of [3H]Ins(1,4,5)P3 and markedly increase [3H]Ins(1,4)P2, but [3H]Ins(1,3,4,5)P4, [3H]Ins(1,3,4)P3 and [3H]Ins(1,3)P2 are virtually unaffected. Ca2(+)-dependent [3H]inositol polyphosphate metabolism may involve different pools of lipids and/or phosphoinositidases.

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Accumulations of cyclic AMP and inositol phosphates in guinea pig cerebral cortical synaptoneurosomes: enhancement by agents acting at sodium channels

Cited by 17 publications

References 23 publications

Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

A Specific Transduction Mechanism for the Glutamate Action on Phosphoinositide Metabolism via the Quisqualate Metabotropic Receptor in Rat Brain Synaptoneurosomes: II. Calcium Dependency, Cadmium Inhibition

Differences between muscarinic-receptor- and Ca2+-induced inositol polyphosphate isomer accumulation in rat cerebral-cortex slices

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Accumulations of cyclic AMP and inositol phosphates in guinea pig cerebral cortical synaptoneurosomes: enhancement by agents acting at sodium channels

Cited by 17 publications

References 23 publications

Ca2+‐Independent, Ca2+‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Ca2+‐Independent, Ca2+‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

A Specific Transduction Mechanism for the Glutamate Action on Phosphoinositide Metabolism via the Quisqualate Metabotropic Receptor in Rat Brain Synaptoneurosomes: II. Calcium Dependency, Cadmium Inhibition

Differences between muscarinic-receptor- and Ca2+-induced inositol polyphosphate isomer accumulation in rat cerebral-cortex slices

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Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane

Ca²⁺‐Independent, Ca²⁺‐Dependent, and Carbachol‐ Mediated Arachidonic Acid Release from Rat Brain Cortex Membrane