Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Morita, Kenichi; North, Richard; Tokimasa, Takayuki

doi:10.1113/jphysiol.1982.sp014444

Cited by 105 publications

(40 citation statements)

References 23 publications

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“…In parasympathetic nerves innervating the guineapig ileum, muscarinic inhibitory receptors have been found in the myenteric plexus (Kilbinger & Wagner, 1979;Morita et al, 1982) in addition to those on the postganglionic neurones (Dzieniszewski & Kilbinger, 1978;Fosbraey & Johnson, 1980). The lung and the gut are derived from the same embryological tissue and many similarities in their innervation have been found, so it is possible that inhibitory muscarinic receptors may have multiple locations in the lung as they do in the ileal innervation.…”

Section: Discussionmentioning

confidence: 99%

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Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

Faulkner

Fryer

Maclagan

1986

British J Pharmacology

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1 The location of neuronal inhibitory muscarinic receptors in pulmonary parasympathetic nerves was investigated in vivo and in vitro. The effects of an agonist for neuronal muscarinic receptors (pilocarpine) and an antagonist (gallamine) were tested on contractions of airway smooth muscle induced by pre-and postganglionic cholinergic nerve stimulation. 2 In anaesthetized guinea-pigs, gallamine potentiated constriction of the tracheal tube and smaller airways induced by preganglionic stimulation. Gallamine also potentiated postganglionic stimulation induced by transmural stimulation of the tracheal tube and by 1-1-dimethyl-4-phenylpiperazinium iodide in the rest of the lung. 3 Bronchoconstriction and contraction of the tracheal tube induced by intravenous acetylcholine were not potentiated by gallamine, indicating that postjunctional muscarinic receptors in airway smooth muscle were not involved in the potentiation. 4 The muscarinic agonist, pilocarpine, had the opposite effect to gallamine and inhibited contractions of the tracheal tube induced by both types of nerve stimulation. 5 In vitro, the inhibitory effect of pilocarpine was demonstrated in the tracheal tube preparation stimulated both pre-and postganglionically. The effect of pilocarpine was antagonized by gallamine. 6 Because gallamine and pilocarpine affected the responses to postganglionic stimulation, the inhibitory muscarinic receptors must be located on the postganglionic neurones of the parasympathetic nerves innervating the trachea and the smaller airways. However, these experiments cannot exclude the possibility that muscarinic receptors may also be located on the soma of the ganglion cells.

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Section: Discussionmentioning

confidence: 99%

“…In these tissues, the receptors are located in the ganglia (Suzuki & Volle, 1979;Gallagher et al, 1982;Morita et al, 1982;Ashe & Yarosh, 1984) and on the postganglionic final nerve terminals (Loffelholz & Muscholl, 1970;Kilbinger & Wagner, 1979;Fox et al, 1985;Wetzel & Brown, 'Author for correspondence. 1985).…”

Section: Introductionmentioning

confidence: 99%

Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

Faulkner

Fryer

Maclagan

1986

British J Pharmacology

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“…It is unlikely that acetylcholine is the mediator of the sEPSPs since sEPSPs were not reduced in amplitude or duration in the presence of atropine but were rather potentiated by atropine. Such an increase in the duration of sEPSPs in the presence of a muscarinic antagonist was also observed in myenteric neurones of the guinea-pig ileum (Morita et al 1982). Although acetylcholine usually has excitatory effects in the enteric nervous system, it has been shown to inhibit, presynaptically, its own release and that of noradrenaline (North et al 1985) and to hyperpolarize submucosal neurones of the guinea-pig caecum (Mihara & Nishi, 1989).…”

Section: Pharmacology Of the Sepspmentioning

confidence: 95%

Characteristics of mucosally projecting myenteric neurones in the guinea‐pig proximal colon

Neunlist

Dobreva

Schemann

1999

The Journal of Physiology

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Neural regulation of a variety of gastrointestinal functions is primarily achieved by the enteric nervous system which is embedded within the gastrointestinal wall. It is usually formed from two major plexus: the myenteric plexus located between the circular and the longitudinal muscle layer and the submucosal plexus situated between the submucosa and the mucosa (for review, see Wood, 1994). In the early part of the 1970s, the first attempt to classify enteric neurones was made using extracellular recording techniques (Wood, 1970). Nishi & North (1973) and Hirst et al. (1974) then used intracellular microelectrode techniques to determine the electrophysiological characteristics of myenteric neurones in the guinea-pig small intestine. Although their classification schemes did not recover exactly the same neuronal populations, two major groups of neurones were revealed. Following the classification of Hirst et al. (1974), S neurones (for synaptically driven) and AH neurones (named after the characteristic long-lasting membrane potential hyperpolarization following the action potential) made up the two populations. Further studies by Wood and his collaborators revealed the presence of different classes of myenteric neurones depending on the region of the gut studied (Wood, 1994). Additionally, enteric neurones may be subdivided into neurochemically distinct populations (Costa et al. 1996), whose number exceeds the broadly defined electrophysiological classes. The use of intracellular injection of biocytin or neurobiotin allowed the morphology of electrophysiologically classified neurones to be determined. AH neurones were extensively studied in the ileum (for review, see Furness et al. 1998) where they were shown to have morphological characteristics of multipolar Dogiel type II neurones with most processes projecting in the circumferential direction (Iyer et al. 1988;Bornstein et al. 1991). Neuronal tracing methods showed

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“…Slow muscarinic cholinergic depolarizations having properties similar to those in BLA pyramidal cells have also been observed in a variety of other neurons in both the central and peripheral nervous systems (for review see North, 1989). In the vast majority of cases, the increase in input resistance and resultant depolarization have been attributed either to the blockade of a potassium leak conductance which contributes to resting membrane potential (IK leak) (Dodd, Dingledine & Kelly, 1981;Benardo & Prince, 1982;Morita, North & Tokimasa, 1982;Madison et al 1987;Benson et al 1988;Greene, Gerber & McCarley, 1989;Pitler & Alger, 1990) or to a reduction in the time-and voltage-dependent conductance, IM Benardo & Prince, 1982;Halliwell & Adams, 1982 (Womble & Moises, 1990). In those experiments, bath application of carbachol was found to block IM directly and also produced an inward shift in holding current when neurons were voltage clamped to negative potentials (beyond -65 mV) where IM is inactivated.…”

Section: Muscarinic Depolarizationmentioning

confidence: 99%

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Washburn

Moises

1992

The Journal of Physiology

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SUMMARY1. Intracellular recordings were obtained from pyramidal-type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain.2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after-hyperpolarization (AHP)that followed a series of current-evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non-cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine-sensitive manner.4. Local application of carbachol to pyramidal cells produced a short-latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium.5. The carbachol-induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice.6. The findings that the carbachol-induced depolarization was associated with an increase in Ri, often had a reversal potential below -80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. M. S. WASHBURN AND H. C MOISES evoked a series of fast EPSPs followed by IPSPs. These non-cholinergic potentials were followed by a slow EPSP that lasted from 10 s-4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calciumdependent release of acetylcholine (ACh).8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.9. The present results provide the first demonstration of muscarinic cholinergic actions in an area of the amygdala known to receive cholinergic innervation. These effects appear to involve both direct and indirect mechanisms.

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Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Cited by 105 publications

References 23 publications

Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

Postganglionic muscarinic inhibitory receptors in pulmonary parasympathetic nerves in the guinea‐pig

Characteristics of mucosally projecting myenteric neurones in the guinea‐pig proximal colon

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

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