Effects of surugatoxin and other nicotinic and muscarinic antagonists on phosphatidylinositol metabolism in active sympathetic ganglia

Pickard, M. R.; Hawthorne, J. N.; Hayashi, Eiichi; Yamada, Shizuo

doi:10.1016/0006-2952(77)90208-8

Cited by 34 publications

(19 citation statements)

References 10 publications

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“…Larrabee and Leicht (1965) have shown that stimulation of the superior cervical ganglion of the rat is associated with an increase in inositol phospholipid metabolism. These observations were confirmed by other investigators (Larrabee et al, 1963;Pickard et al, 1977;Briggs et al, 1985a), who concluded that during orthodromic nerve stimulation, inositol lipid metabolism is activated.…”

supporting

confidence: 82%

“…Hence, the rate of release of [3H]inositol from prelabeled phosphorylated inositol derivatives can be used as a sensitive indicator of changes in turnover rate of inositol phospholipids (Berridge and Fain, 1979;Berridge and Irvine, 1984;Berridge and Rubio, 1986). In mammalian sympathetic ganglia, electrical stimulation (Hokin, 1965(Hokin, , 1966Larrabee and Leicht, 1965;Pickard et al, 1977;Briggs et al, 1985a,b), cholinergic activation (Hokin, 1966;Patterson and Volle, 1984;Bone and Michell, 1985), K+ depolarization (Bone and Michell, 1 985), and 4-aminopyridine administration (Patterson and Volle, 1984) all result in "activation of inositol lipid metabolism," i.e., all resulted in changes in contents of the various inositol derivatives. These findings are in agreement with our observation that orthodromic agonist stimulation of the frog sympathetic ganglion is associated with an increase in [3H]inositol metabolism that persists after the stimulation is terminated.…”

Section: Two-ganglia Experiments: Production Of a Diffusible Substancmentioning

confidence: 99%

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Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Rubio

Bencherif

Berne

1989

Journal of Neurochemistry

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The metabolic pathway of inositol phospholipids represents a series of synthetic and hydrolytic reactions with inositol as a by-product. Hence, the rate of [3H]inositol release from prelabeled phospholipids can be used as a reflection of activity of this pathway. In the frog sympathetic ganglion prelabeled with [3H]inositol, we studied the effect of synaptic activity (orthodromic stimulation) on release of 3H-label into the medium. This release was interpreted as [3H]inositol release. The value was low at rest and increased significantly by 32% during orthodromic stimulation (20 Hz for 5 min). However, on cessation of the stimulation, [3H]inositol release increased rapidly by 148% and remained elevated for at least 45 min. This increase in [3H]inositol release during and after the stimulation period was reduced by suffusion of the ganglia with adenosine. We hypothesized that synaptic activation releases a long-lasting stimulatory agonist and a short-lasting inhibitory (adenosine) agonist or agonists affecting [3H]inositol release. To demonstrate the presence of a stimulatory agonist, two sympathetic ganglia were used. One was prelabeled with [3H]inositol, and the other was not. The two ganglia were placed together in a 5-microliter droplet of Ringer's solution containing atropine. Orthodromic stimuli applied to the nonlabeled ganglion elicited release of [3H]inositol from the nonstimulated ganglion. To test whether the adenosine formed during orthodromic stimulation inhibits [3H]inositol release, we destroyed endogenous adenosine by suffusion of the ganglia with adenosine deaminase during the stimulation period. We found that adenosine deaminase induced large increases in [3H]inositol release during the stimulation period, in contrast to an increase seen only during the poststimulation period when adenosine deaminase was omitted. Because [3H]inositol release is assumed to parallel changes in content of inositol phosphates, we anticipated no changes of the levels of these compounds during orthodromic stimulation. However, measurements showed that levels of inositol phosphates and inositol phospholipids were all elevated except for phosphatidylinositol 4-phosphate. On termination of the stimulus, they remained elevated, with a further increase in levels of inositol trisphosphate and phosphatidylinositol 4-phosphate. We conclude that endogenous adenosine inhibits [3H]inositol release, possibly by modulating several of the steps of the inositol phospholipid pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

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confidence: 82%

Section: Two-ganglia Experiments: Production Of a Diffusible Substancmentioning

confidence: 99%

Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Rubio

Bencherif

Berne

1989

Journal of Neurochemistry

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“…This is in contrast to the results obtained in the slices of rat cerebral cortex, where K+ or veratrine stimulation of InsP accumulation could be greatly enhanced by physostigmine and where this effect was suppressed by atropine (Kendall and Nahorski, 1987;Baird and Nahorski, 1989). Depolarization has also been shown to stimulate the metabolism of inositol phospholipid in the superior cervical ganglion which, at least in part, can be suppressed by muscarinic receptor antagonists (Pickard et al, 1977;Bone and Michell, 1985). Depolarizing stimuli, such as elevated extracellular K+ or Na+-channel activation, are also known to induce InsP formation in cere-bra1 preparations Nahorski, 1984, 1985;Batty et al, 1985;Candy et al, 1985;Court et al, 1986;Eva and Costa, 1986;Rooney and Nahorski, 1986;Zernig et al, 1986;Gurwitz and Sokolovsky, 1987;Maier and Rutledge, 1987;Weiss et al, 1988;Nahorski, 1989, 1990u,b), synaptoneurosomes (Gusovsky et al, 1986;Gusovsky and Daly, 1988), synaptosomes (Habermann and L u x , 1986;Audigier et al, 1988), ganglia (Bone and Michell, 1985;Briggs et al, 1985), and other tissues, including smooth muscle (Best and Bolton, 1986;Sasaguri and Watson, 1988), pancreatic islets (Biden et al, 1987), andheart (McDonough et al, 1988).…”

Section: Discussionmentioning

confidence: 59%

Effects of Muscarinic Agonists and Depolarizing Agents on Inositol Monophosphate Accumulation in the Rabbit Vagus Nerve

Sierro

Vitus

Dunant

1992

Journal of Neurochemistry

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The effects of muscarinic agonists and depolarizing agents on inositol phospholipid hydrolysis in the rabbit vagus nerve were assessed by the measurement of [3H]inositol monophosphate production in nerves that had been preincubated with [3H]inositol. After 1 h of drug action, carbachol, oxotremorine, and arecoline increased the inositol monophosphate accumulation, though the maximal increase induced by these agonists differed. Addition of the muscarinic antagonists atropine or pirenzepine shifted the carbachol dose-response curves to the right, without decreasing the carbachol maximal stimulatory effects. The KB for pirenzepine was 35 nM, which is characteristic of muscarinic high-affinity binding sites coupled to phosphoinositide turnover and often associated with the M1 receptor subtype. On the other hand, agents known to depolarize or to increase the intracellular Ca2+ concentration, e.g., elevated extracellular K+, ouabain, Ca2+, and the Ca2+ ionophore A23187, also increased inositol monophosphate accumulation. These effects were not mediated by the release of acetylcholine, as suggested by the fact that they could not be potentiated by the addition of physostigmine nor inhibited by the addition of atropine. The Ca(2+)-channel antagonist Cd2+, also known to inhibit the Na+/Ca2+ exchanger, was able to block the effects of K+ and ouabain, but did not alter those of carbachol. These results suggest that depolarizing agents increase inositol monophosphate accumulation in part through elevation of the intracellular Ca2+ concentration and that muscarinic receptors coupled to phosphoinositide turnover are present along the trunk of the rabbit vagus nerve.

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“…It is conceivable that some of the reported multiple modes of action of ACh in sympathetic ganglia [Larabee and Leicht, 1965;Larabee, 1968;Lapetina et al, 1976;Pickard et al, 1977;Greene and Rein, 1978;Ikeno et al, 1981;Ip et al, 1982;Morita et al, 1982;Bone et al, 1984;Bone and Michell, 1985;Briggs et al, 1985;Brown and Selyanko, 19851 may not be primarily linked to the direct activation of subsynaptic nicotinic receptors. Therefore, the presence of cholinesterases (ChEs) on various ultrastructural sites outside of the nicotinic synapses could be expected.…”

Section: Introductionmentioning

confidence: 99%

Recovery of cholinesterases in soman‐injected superior cervical ganglion of the rat in the presence and absence of innervation

Klinar

Brzin

1987

J of Neuroscience Research

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We have previously described the procedure for quantitative separation of extracellular and intracellular ChEs using mild treatment of rat superior cervical ganglion with papain. Here, this procedure was used in order to investigate the recovery of ChEs in the two pools after irreversible inhibition by soman which was directly injected into the ganglion. After such treatment only ganglion ChEs were totally inhibited, whereas the activity of ChEs in preganglionic neurons and their axons remained unaffected. Comparing in innervated and decentralized ganglia the pattern of recovery rate and ultrastructural reappearance of ChEs after local inhibition, with that reported after systemic ChEs inhibition, it was possible to distinguish between the indirect effects of innervation on the recovery rate and pattern of ChEs of ganglion origin and the direct contribution to the total ganglion enzyme activity of ChEs originating in the preganglionic elements.The absence of nerve contracts affects mostly extracellular activity, particularly AChE, whereas the intracellular activity of AChE was only slightly decreased and the activity of nsChE was somewhat increased. This increase coincides with the enhanced cytochemical reaction of nsChE in some nonneuronal cells in the ganglion.Actinomycyn D decreased the rate of initial rapid phase of recovery of intracellular ChEs when injected in the ganglion daily for three days, whereas the recovery of extracellular ChEs was already decreased the first day of Actinomycyn D application. This indicates that the externalization of the enzyme is more affected than its synthesis by inhibition the translation step.The results further suggest that functional innervation of the ganglion down-regulate the rate of reappearance of the new enzyme at the extracellular and intracellular locations and changes the ratio between AChE and nsChE. ChEs synthesized in preganglionic neurons begins to contribute directly to the total ganglion ChEs activity in the late stages of enzyme recovery in spite of the presence of the preganglionic ChEs @ 1987 Alan R. Liss, Inc.which was not inhibited after intraganglionic injection of soman. This finding suggests that the externalization and extracellular attachment of ChEs and not their preganglionic resynthesis may be the cause for delayed reappearance of ChEs affiliated with nerve terminals in the ganglion.

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Effects of surugatoxin and other nicotinic and muscarinic antagonists on phosphatidylinositol metabolism in active sympathetic ganglia

Cited by 34 publications

References 10 publications

Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Inositol Phospholipid Metabolism During and Following Synaptic Activation: Role of Adenosine

Effects of Muscarinic Agonists and Depolarizing Agents on Inositol Monophosphate Accumulation in the Rabbit Vagus Nerve

Recovery of cholinesterases in soman‐injected superior cervical ganglion of the rat in the presence and absence of innervation

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