Heteroreceptor-mediated modulation of noradrenaline and acetylcholine release from peripheral nerves

Fuder, H.; Muscholl, E.

doi:10.1007/bfb0049778

Cited by 102 publications

(73 citation statements)

References 496 publications

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“…In addition, these drugs inhibit the depolarization evoked release of acetylcholine via stimulation of different subtypes of presynaptic receptors, i.e. 5-HTlA-, NKI-, GABAB-, M3-receptors (for review, see Fuder & Muscholl, 1995). The biphasic modulation by NO donors of acetylcholine release as presented in this paper is in agreement with recent observations of a NO donor-mediated increase of basal and inhibition of evoked release of dopamine from PC12 cells (Sun et al, 1995), and the facilitation and inhibition by SIN-1 of acetylcholine release at cholinergic synapses of Aplysia (Meulemans et al, 1995).…”

Section: Resultsmentioning

confidence: 99%

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Hebeiss

Kilbinger

1996

British J Pharmacology

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1 The effects of the nitric oxide (NO) donors, 3-morpholino-sydnonimine (SIN-1), S-nitroso-Nacetylpenicillamine (SNAP) and sodium nitroprusside on basal and electrically evoked release of [3H]-acetylcholine were studied in myenteric plexus longitudinal muscle preparations of the guinea-pig small intestine preincubated with [3H]-choline. 4 It is concluded that NO stimulates basal acetylcholine release from myenteric neurones through activation of guanylyl cyclase. In addition, NO inhibits the depolarization evoked release of acetylcholine by a presynaptic mechanism unrelated to cyclic GMP. The data imply that NO is not only an inhibitory transmitter to intestinal smooth muscles but also a modulator of cholinergic neurotransmission in the myenteric plexus.

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Section: Resultsmentioning

confidence: 99%

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Hebeiss

Kilbinger

1996

British J Pharmacology

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“…Studies of radiolabeled NE overflow from sympathetic neurons and of junctional currents in target cells show that NE secretion can be modulated by several neurotransmitters (see ref. 15 for review).…”

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confidence: 99%

Modulation by neurotransmitters of catecholamine secretion from sympathetic ganglion neurons detected by amperometry

Koh

Hille

1997

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

108

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Many neuromodulators inhibit N-type Ca 2؉ currents via G protein-coupled pathways in acutely isolated superior cervical ganglion (SCG) neurons. Less is known about which neuromodulators affect release of norepinephrine (NE) at varicosities and terminals of these neurons. To address this question, we used carbon fiber amperometry to measure catecholamine secretion evoked by electrical stimulation at presumed sites of high terminal density in cultures of SCG neurons. The pharmacological properties of action potential-evoked NE release paralleled those of N-type Ca 2؉ channels: Release was completely blocked by Cd 2؉ or -conotoxin GVIA, reduced 50% by 10 M NE or 62% by 2 M UK-14,304, an ␣ 2 -adrenergic agonist, and reduced 63% by 10 M oxotremorine M (Oxo-M), a muscarinic agonist. Consistent with action at M 2 or M 4 receptor subtypes, Oxo-M could be antagonized by 10 M muscarinic antagonists methoctramine and tropicamide but not by pirenzepine. After overnight incubation with pertussis toxin, inhibition by UK-14,304 and Oxo-M was much reduced. Other neuromodulators known to inhibit Ca 2؉ channels in these cells, including adenosine, prostaglandin E 2 , somatostatin, and secretin, also depressed secretion by 34-44%. In cultures treated with -conotoxin GVIA, secretion dependent on L-type Ca 2؉ channels was evoked with long exposure to high K ؉ Ringer's solution. This secretion was not sensitive to UK-14,304 or Oxo-M. Evidently, many neuromodulators act on the secretory terminals of SCG neurons, and the depression of NE release at terminals closely parallels the membrane-delimited inhibition of N-type Ca 2؉ currents in the soma.Patch-clamp technique studies have shown that N-type Ca 2ϩ channels of the cell soma are modulated via many different G protein-coupled neurotransmitter receptors in superior cervical ganglion (SCG) neurons (1-6; for review, see ref. 7). Many neurotransmitter receptors, including ␣ 2 -adrenergic, somatostatin, prostaglandin E 2 (PGE 2 ), adenosine, M 4 muscarinic, pancreatic polypeptide, secretin, vasoactive intestinal peptide, and substance P, inhibit by a fast, membrane-delimited mechanism (7). Angiotensin II receptors and M 1 muscarinic receptors inhibit Ca 2ϩ channels via a slow, diffusible cytoplasmic messenger.Despite intensive work dissecting different modulatory pathways and investigating their underlying mechanisms (7-9), definite physiological roles for Ca 2ϩ channel inhibition in SCG cells have not yet been determined. Two have been proposed (7, 10): (i) In the soma, inhibition of Ca 2ϩ entry could alter cell excitability and action potential firing patterns because the somata possess Ca 2ϩ -activated K ϩ channels and Ca 2ϩ -sensitive M-type K ϩ channels (11-13), and (ii) at sympathetic nerve terminals and varicosities, inhibition of Ca 2ϩ influx could decrease norepinephrine (NE) secretion, as in Dunlap and Fischbach's (14) general concept of presynaptic inhibition. This hypothesis would require that N-type Ca 2ϩ channels be functionally coupled to many receptors at the dist...

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“…The presence of prejunctional muscarinic heteroreceptors on sympathetic nerves is well established (Fuder & Muscholl 1995). Acetylcholine and other muscarinic agonists inhibit noradrenaline release evoked by stimulation of postganglionic nerves in many tissues, including blood vessels (Rand & Story 1991).…”

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confidence: 99%

Prejunctional Muscarinic Receptor Modulation of Noradrenaline Release from Sympathetic Neurones in Rabbit Aorta ^*

Lomholt¹,

Nedergaard²

2000

Pharmacology & Toxicology

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Abstract:The prejunctional muscarinic modulation of stimulation-evoked release of 3 H-noradrenaline from sympathetic neurones in rabbit aorta was examined. The role of transmitter uptake, a-adrenoceptor blockade, stimulation frequency and endothelium on the modulation was investigated. Rings of aorta were incubated with (-)-3 H-noradrenaline and subsequently subjected to electrical-field stimulation. Fractional H-noradrenaline is (1) inversely related to stimulation frequency; (2) independent of endothelium; (3) unaffected by neuronal and extraneuronal transmitter uptake; (4) that cocaine is not a prejunctional muscarinic antagonist; (5) that cocaine, but not desipramine, is suited as a neuronal uptake inhibitor in studies of prejunctional muscarinic receptor subtypes; and (6) and that there is an inverse interaction between prejunctional a 2 -adrenoceptors and muscarinic receptors.

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Heteroreceptor-mediated modulation of noradrenaline and acetylcholine release from peripheral nerves

Cited by 102 publications

References 496 publications

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Modulation by neurotransmitters of catecholamine secretion from sympathetic ganglion neurons detected by amperometry

Prejunctional Muscarinic Receptor Modulation of Noradrenaline Release from Sympathetic Neurones in Rabbit Aorta ^*

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Heteroreceptor-mediated modulation of noradrenaline and acetylcholine release from peripheral nerves

Cited by 102 publications

References 496 publications

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Modulation by neurotransmitters of catecholamine secretion from sympathetic ganglion neurons detected by amperometry

Prejunctional Muscarinic Receptor Modulation of Noradrenaline Release from Sympathetic Neurones in Rabbit Aorta *

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Prejunctional Muscarinic Receptor Modulation of Noradrenaline Release from Sympathetic Neurones in Rabbit Aorta ^*