The regulation of cyclic nucleotides in a sympathetic ganglion

Volle, Robert L.; Quenzer, Linda F.; Patterson, Brian A.

doi:10.1016/0165-1838(82)90023-6

Cited by 17 publications

(3 citation statements)

References 18 publications

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“…Ip et al (16) Hz. Immediately after stimulation, the ganglia were homogenized in 3%c trichloroacetic acid and the precipitated material was subjected to two-dimensional gel electrophoresis (25) (29,30), and agents that raise cAMP levels in the ganglion can cause activation and phosphorylation of tyrosine hydroxylase (20,21). Several peptides, including vasoactive intestinal peptide and secretin, also increase the content of cAMP in the ganglion (20,31 Preganglionic nerve stimulation increased the phosphorylation of at least six proteins other than tyrosine hydroxylase in the SCG.…”

Section: Discussionmentioning

confidence: 99%

Electrical stimulation increases phosphorylation of tyrosine hydroxylase in superior cervical ganglion of rat.

Cahill¹,

Perlman²

1984

Proc. Natl. Acad. Sci. U.S.A.

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Electrical stimulation of the superior cervical ganglion of the rat increased the phosphorylation of tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) in this tissue. Ganglia were incubated with [32pJp1 for 90 min and were then electrically stimulated via the preganglionic nerve. Tyrosine hydroxylase was isolated from homogenates of the ganglia by immunoprecipitation followed by polyacrylamide gel electrophoresis. 32P-labeled tyrosine hydroxylase was visualized by radioautography, and the incorporation of 32p into the enzyme was quantitated by densitometry of the radioautograms. Stimulation of ganglia at 20 Hz for 5 min increased the incorporation of 32p into tyrosine hydroxylase to a level 5-fold that found in unstimulated control ganglia. The increase in phosphorylation of tyrosine hydroxylase was dependent on the duration and frequency of stimulation. Preganglionic stimulation did not increase the phosphorylation of tyrosine hydroxylase in a medium that contained low Ca2+ and high Mg2 . Increases in phosphorylation were reversible; within 30 min after the cessation of stimulation, the incorporation of 32p into tyrosine hydroxylase decreased to the level found in unstimulated ganglia. The nicotinic antagonist hexamethonium reduced the increase in 32p incorporation into tyrosine hydroxylase by about 50%, while the muscarinic antagonist atropine had no effect. Thus, preganglionic stimulation appeared to increase the phosphorylation of tyrosine hydroxylase in part by a nicotinic mechanism and in part by a noncholinergic mechanism. Antidromic stimulation of ganglia also increased the phosphorylation of tyrosine hydroxylase. Two-dimensional gel electrophoresis revealed that electrical stimulation also increased the incorporation of 32p into at least six other phosphoproteins in the ganglion.Electrical stimulation of sympathetic nerves increases the rate of catecholamine biosynthesis in these nerves (1). This acceleration of catecholamine synthesis was initially thought to be due to the release of catecholamines from the nerve terminals, resulting in a decrease in intraneuronal catecholamine levels and a relief of the feedback inhibition of tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) by catecholamines (2). It is now clear, however, that stimulation of both peripheral and central adrenergic nerves causes a stable activation of tyrosine hydroxylase and a change in the kinetic properties of the enzyme (most commonly, a decrease in the apparent Km for pteridine cofactor and an increase in the Ki for catecholamines) (3-6). There is evidence that the activation of tyrosine hydroxylase may be mediated by phosphorylation of the enzyme. Tyrosine hydroxylase is a phosphoprotein (7) and can be activated in vitro by phosphorylation (8-12). Moreover, phosphorylation of tyrosine hydroxylase is increased in situ in adrenal chromaffin cells by stimuli that increase the rate of catecholamine synthesis in these cells (13,14).Preganglionic stimulation increases tyrosine hydroxylase activity in the...

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Section: Discussionmentioning

confidence: 99%

Electrical stimulation increases phosphorylation of tyrosine hydroxylase in superior cervical ganglion of rat.

Cahill¹,

Perlman²

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…Regulation by cyclic AMP Both preganglionic tetani and isoprenaline increase cyclic AMP levels in the ganglion (Briggs et al, 1982;Volle et al, 1982), potentiate nicotinic transmission, and potentiate evoked ACh release. We therefore tested the hypothesis that cyclic AMP mediates l.t.p.…”

Section: Receptor-mediated Regulationmentioning

confidence: 99%

“…The idea that cyclic AMP may mediate the 3-adrenoceptor-induced potentiation of nicotinic transmission is prompted by several findings: (1) P-adrenoceptor agonists stimulate cyclic AMP synthesis potently and efficaciously in the whole sympathetic ganglion (Briggs et al, 1982;Volle et al, 1982); (2) preganglionic denervation reduces the amount of cyclic AMP formed following exposure to ,-adrenoceptor agonists (Quenzer et al, 1980); (3) P-adrenoceptor agonists and cyclic AMP both increase the quantal content of nicotinic transmission in the frog sympathetic ganglion (Kuba & Kumamoto, 1986), and both increase nicotinic transmission and evoked ACh release in the rat sympathetic ganglion (this study). However, other evidence indicates that Padrenoceptor agonists may also act postsynaptically in the sympathetic ganglion (Brown & Dunn, 1983a), and that the potentiation is not mediated by cyclic AMP (Brown & Dunn, 1983b (Lynch & Baudry, 1984;Stanton & Sarvey, 1985a,b;Akers et al, 1986;Malenka et al, 1986), there is persuasive evidence in Aplysia that cyclic AMP mediates a longlasting presynaptic potentiation through inhibition of K+ channels (Kandel & Schwartz, 1982;Abrams et al, 1984;Schuster et al, 1985;Walters & Byrne, 1985; cf.…”

Section: Receptor-mediated Regulationmentioning

confidence: 99%

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Briggs

McAfee

McCaman

1988

British J Pharmacology

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1 Using the rat superior cervical ganglion in vitro, the relative efficacy of nicotinic synaptic transmission was estimated by recording the postganglionic compound action potential and the amount of endogenous acetylcholine (ACh) released. These two parameters were correlated in individual ganglia by sampling the bathing medium for the assay of ACh while simultaneously recording the postganglionic response.2 The P-adrenoceptor agonist isoprenaline potentiated both the evoked release of ACh and the postganglionic response by about 20% during preganglionic stimulation at 0.2 Hz. 3 The adenosine receptor agonist 2-chloroadenosine inhibited ACh release and the postganglionic response by about 35%. 4 Tetanic preganglionic stimulation for a few seconds induced a long-term potentiation of nicotinic responses and of ACh release. Both of these potentiations were dependent upon extracellular Ca2l during the tetani. 5 Forskolin and analogues of cyclic AMP also caused a long-lasting potentiation of both the evoked release ofACh and the postganglionic response, indicating that cyclic AMP may regulate transmission by a presynaptic mechanism. The specificity of the cyclic AMP analogues was tested using various butyryl-and bromo-purine nucleotides. 6 The effects of forskolin and 8-bromo-cyclic AMP did not appear to be dependent upon extracellular Ca2+. 7 The potentiation caused by forskolin was consistently augmented by three phosphodiesterase inhibitors -AH 21-132, papaverine and SQ 20-006. However, the effect of forskolin was not consistently enhanced by theophylline, nor was it reduced by the adenylate cyclase inhibitor SQ 22-536. 8 The neurogenic long-term potentiation was augmented by two of the phosphodiesterase inhibitors that also augmented the forskolin-induced potentiation -papaverine and SQ 20-006. 9 It was concluded that cyclic AMP can enhance nicotinic transmission, and can do so by increasing the evoked release of ACh. However, it was not possible to prove that cyclic AMP mediates the longterm potentiation induced by tetanic preganglionic stimulation.

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Mediation of Nonclassical Postsynaptic Responses by Cyclic Nucleotides

Libet

1988

Neurotransmitters and Cortical Function

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The regulation of cyclic nucleotides in a sympathetic ganglion

Cited by 17 publications

References 18 publications

Electrical stimulation increases phosphorylation of tyrosine hydroxylase in superior cervical ganglion of rat.

Electrical stimulation increases phosphorylation of tyrosine hydroxylase in superior cervical ganglion of rat.

Long‐term regulation of synaptic acetylcholine release and nicotinic transmission: the role of cyclic AMP

Mediation of Nonclassical Postsynaptic Responses by Cyclic Nucleotides

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