Presence of cholinergic neurons in the vagal afferent system: Biochemical and immunohistochemical approaches

Ternaux, Jean‐Pierre; Falempin, Maurice; Palouzier, B.; Chamoin, M.-C.; Portalier, P.

doi:10.1016/0165-1838(89)90151-3

Cited by 30 publications

(18 citation statements)

References 29 publications

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“…Given the paucity of identified propriobulbar inputs to the NTS c, the question arises as to whether vagal afferents themselves are cholinergic. ChAT immunoreactivity has been demonstrated in nodose ganglionic perikarya [21,22], and cross-innervation experiments in rabbits have further corroborated the potential cholinergic function of nodose ganglionic cells receiving esophageal input [23]. However, anatomical and pharmacological data, discussed below, are also consistent with a propriobulbar source of cholinergic NTSc afferents.…”

Section: Connectivity Of the Medullary Esophagomotor Pathwaysmentioning

confidence: 65%

The brainstem esophagomotor network pattern generator: A rodent model

Bieger

1993

Dysphagia

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The evidence reviewed in this essay supports the following working model of the central function generator for esophageal peristalsis in the rat: solitarial subnucleus centralis (NTSc) neurons operate in a dual capacity as esophagomotor reflex interneurons and as command neurons programming respective outputs from nucleus ambiguus compact formation (AMBc) motoneurons during secondary and primary peristalsis. In both conditions, there is a critical requirement for cholinergic input which enables NTSc neurons to generate the timed sequence of AMBc motoneuronal activity. In primary peristalsis, the cholinergic coupling mechanism is activated centrally, probably via projections from deglutitive premotor neurons to the parvicellular reticular formation and thence to the NTS. In reflex (or secondary) peristalsis, the cholinergic input could in part be generated by cholinergic vagal viscerosensory fibers innervating the esophagus. Postulated connections between NTS deglutitive neurons and the parvicellular cholinergic neurons of the intermediate reticular formation have yet to be demonstrated. Premotor input from NTSc to AMBc is generated by somatostatinergic and excitatory aminoacidergic neurons. Coactivation of both inputs by cholinergic afferents is necessary to generate esophagomotor output from AMBc neurons. The model under study is derived from investigations into central mechanisms governing striated muscle peristaltic activity. Whether the basic operational principles revealed thus far apply to peristaltic pattern generation in species with a smooth muscle esophagus, requires further investigation.

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Section: Connectivity Of the Medullary Esophagomotor Pathwaysmentioning

confidence: 65%

The brainstem esophagomotor network pattern generator: A rodent model

Bieger

1993

Dysphagia

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“…The vagal nerve has stimulatory and inhibitory actions on acid secretion [20,21] and it releases several neurotransmitters, such as acetylcholine [22], gastrin-releasing peptide (GRP) [23], substance P [24], calcitonin gene-related peptide [24], and pituitary adenylate cyclase activating peptide (PACAP) [25]. Among these, GRP has a stimulatory action on gastrin release from G cells [26].…”

Section: Discussionmentioning

confidence: 99%

Histamine Mediates the Stimulatory Action of Ghrelin on Acid Secretion in Rat Stomach

Yakabi

Onouhi

et al. 2006

Dig Dis Sci

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Ghrelin, a novel growth hormone-releasing peptide, is present in the rat and human stomach and is known to stimulate acid secretion and stomach motility. However, the mechanism of action of ghrelin is not fully understood. In the present study, we attempted to elucidate the role of histamine in ghrelin-induced acid secretion in rat stomach. Intravenous administration of ghrelin at 0.8 to 20 microg/kg dose dependently increased gastric acid secretion, as measured by the gastric lumen perfusion method. The maximum response was almost equal to that of gastrin (20 microg/kg). These actions were abolished by bilateral subdiaphragmatic vagotomy. Famotidine (0.33 mg/kg) also completely inhibited the effects of ghrelin. Furthermore, ghrelin increased histidine decarboxylase (HDC) messenger RNA (mRNA) levels, as measured by real-time reverse transcription-polymerase chain reaction using LightCycler. The action of ghrelin on HDC mRNA was abolished by vagotomy. Ghrelin did not affect histamine release from isolated vascularly perfused rat stomach. Taken together, these results suggest that ghrelin stimulates gastric acid secretion via a mechanism involving activation of vagal efferent nerve and histamine release from gastric enterochromaffin-like cells.

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“…These nerve fibres run within the mesenteric nerves and may represent axons of preganglionic parasympathetic cholinergic neurons (Berthoud et al 1991), postganglionic cholinergic sympathetic neurons, axon collaterals of the intestinofugal neurons (a proportion of which are likely to be cholinergic; Szurszewski and King 1989;Mann et al 1995;current results), or axons of extrinsic sensory neurons. Not all spinal sensory neurons supplying the intestine contain CGRP (Dockray et al 1991), and there is evidence that a proportion of both spinal and vagal sensory neurons may contain ChAT (Palouzier et al 1987;Ternaux et al 1989;Palouzier Paulignan et al 1991;Sann et al 1995).…”

Section: Nature Of Labelled Nerve Fibresmentioning

confidence: 98%

Rapid anterograde and retrograde tracing from mesenteric nerve trunks to the guinea-pig small intestine in vitro

Tassicker

Hennig²,

Costa³

et al. 1999

Cell and Tissue Research

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A novel technique for rapid anterograde labelling of cut axons in vitro was used to visualise the peripheral branches of mesenteric nerve trunks supplying the guinea-pig small intestine. Biotinamide, dissolved in an artificial intracellular solution, was applied to the cut ends of the mesenteric nerves and the tissue was maintained in organ culture overnight. Labelled nerve fibres were visualised by fluorescein isothiocyanate (FITC)-conjugated streptavidin. Intense staining of nerve fibres and terminal varicosities in the ganglia and internodal strands of the myenteric plexus was achieved up to 15 mm from the application site. Filled fibres formed baskets around some myenteric nerve cell bodies, suggesting target-specific neurotransmission. When combined with multiple-labelling immunohistochemistry for tyrosine hydroxylase (TH), calcitonin gene-related protein (CGRP) or choline acetyltransferase (ChAT), most anterogradely labelled nerve fibres, and many pericellular baskets, were found to be TH immunoreactive, indicating their postganglionic sympathetic origin. Double-labelling immunohistochemistry revealed that the postganglionic sympathetic pericellular baskets preferentially surrounded 5-hydroxytryptamine (5-HT)-handling myenteric neurons. Some biotinamide-filled fibres were CGRP immunoreactive, and are likely to originate from spinal sensory neurons. We describe for the first time many pericellular baskets labelled from the mesenteric nerves which were ChAT immunoreactive. Retrogradely filled intestinofugal nerve cell bodies were also observed, all of which had a single axon arising from a small nerve cell body with short filamentous or lamellar dendrites. Many of these cells were ChAT immunoreactive. This in vitro technique is effective in identifying the fine arrangement of nerve terminals arising from nerve trunks in the periphery.

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Presence of cholinergic neurons in the vagal afferent system: Biochemical and immunohistochemical approaches

Cited by 30 publications

References 29 publications

The brainstem esophagomotor network pattern generator: A rodent model

The brainstem esophagomotor network pattern generator: A rodent model

Histamine Mediates the Stimulatory Action of Ghrelin on Acid Secretion in Rat Stomach

Rapid anterograde and retrograde tracing from mesenteric nerve trunks to the guinea-pig small intestine in vitro

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