Gastro-oesophageal afferent and serotonergic inputs to vagal efferent neurones

La, Blackshaw

doi:10.1016/0165-1838(94)90129-5

Cited by 10 publications

(6 citation statements)

References 22 publications

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“…We propose that this functional independence occurs via coding of NTS neurons based on the gastric vagal afferent subtype they receive, and on the distinct pool of gastric motorneurons to which they project 42,43 . However, intense activation of mucosal afferents with CCK or 5‐HT does result in convergent effects on vagal motorneurons responsive to gastric distension 31,44,45 . This may be a reflection of the central termination of both vagal afferent subtypes in the same subnucleus, which we suggest remain functionally independent until summated.…”

Section: Discussionmentioning

confidence: 80%

“…42,43 However, intense activation of mucosal afferents with CCK or 5-HT does result in convergent effects on vagal motorneurons responsive to gastric distension. 31,44,45 This may be a reflection of the central termination of both vagal afferent subtypes in the same subnucleus, which we suggest remain functionally independent until summated.…”

Section: Gastric Afferent Populations In Nodose Gangliamentioning

confidence: 75%

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Chemical coding and central projections of gastric vagal afferent neurons

Young

Cooper

Blackshaw

2008

Neurogastroenterology Motil

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Vagal afferents that innervate gastric muscle or mucosa transmit distinct sensory information from their endings to the nucleus of the tractus solitarius (NTS). While these afferent subtypes are functionally distinct, no neurochemical correlate has been described and it is unknown whether they terminate in different central locations. This study aimed to identify gastric vagal afferent subtypes in the nodose ganglion (NG) of ferrets, their terminal areas in NTS and neurochemistry for isolectin-B4 (IB4) and calcitonin gene-related peptide (CGRP). Vagal afferents were traced from gastric muscle or mucosa and IB4 and CGRP labelling assessed in NG and NTS. 7 +/- 1% and 6 +/- 1% of NG neurons were traced from gastric muscle or mucosa respectively; these were more likely to label for CGRP or for both CGRP and IB4 than other NG neurons (P < 0.01). Muscular afferents were also less likely than others to label with IB4 (P < 0.001). Less than 1% of NG neurons were traced from both muscle and mucosa. Central terminals of both afferent subtypes occurred in the subnucleus gelatinosus of the NTS, but did not overlap completely. This region also labelled for CGRP and IB4. We conclude that while vagal afferents from gastric muscle and mucosa differ little in their chemical coding for CGRP and IB4, they can be traced selectively from their peripheral endings to NG and to overlapping and distinct regions of NTS. Thus, there is an anatomical substrate for convergent NTS integration for both types of afferent input.

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Section: Discussionmentioning

confidence: 80%

Section: Gastric Afferent Populations In Nodose Gangliamentioning

confidence: 75%

Chemical coding and central projections of gastric vagal afferent neurons

Young

Cooper

Blackshaw

2008

Neurogastroenterology Motil

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“…Other receptors have also been identified, 5-hydroxytryptamine-4 and -3 receptors (5-HT 4 , 5-HT 3 ) have been found on vagal afferent neurons from the upper gastrointestinal tract. Upon activation of 5-HT 4 receptors, neurotransmitters are released from the enteric nerves, thus increasing contractility and stimulation of the peristaltic reflex, whereas 5-HT 3 receptors do not appear to alter vagal efferent activity in response to gastric distension [28,29]. Excitatory and inhibitory neurotransmitters act by modulating the effect of sympathetic and parasympathetic nerve supplies on motor function of sphincter and non-sphincteric muscles.…”

Section: Evolving Concepts In Neural Control Of the Lower Oesophagealmentioning

confidence: 99%

New insights into the treatment of gastroesophageal reflux disease

Campo

2002

Expert Opinion on Therapeutic Patents

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“…As 5-HT is known to excite vagal pathways powerfully, 21,22 i.c. injection of 5-HT (10 mg) served as a positive control experiment to verify effective delivery of drugs to vagal nuclei accessed by cerebrospinal fluid in the 4th ventricle.…”

Section: Effect Of 5-ht On Cck-8-stimulated Pyloric Motilitymentioning

confidence: 99%

Pyloric motor response to central and peripheral nitric oxide in the ferret

Lingenfelser

Blackshaw

Sun

1997

Neurogastroenterology Motil

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This study has investigated the relative importance of central nervous and peripheral nitroxidergic mechanisms in the control of pyloric motility. In 10 urethane-anaesthetized ferrets, drugs were administered directly to the CNS via a 0.5-mm-diameter cannula inserted into the 4th ventricle, approximately at the obex. Drugs were also given directly to the upper GI tract by close intra-arterial (i.a.) injection at the coeliac axis. Antropyloroduodenal pressures were recorded with a five-channel sleeve/sidehole micromanometric assembly (1.35 x 1.75 mm o.d.), which was introduced via the duodenum. Pyloric motility was stimulated throughout the main part of each study with a continuous i.v. infusion of CCK-8 (30 pmol min-1). This infusion produced an immediate and sustained increase in tonic and phasic pyloric activity, and sustained abolition of antral pressure waves. CCK-8 also induced a duodenal motor response, but this was short-lived (11.4 +/- 7.9 min). Coeliac axis injection of the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) decreased phasic pyloric activity (from 330 +/- 35 to 148 +/- 21 mmHg min-1 after SNAP 5 micrograms, P < 0.01). By comparison central SNAP administration over the same dose range had no effect on CCK-stimulated pyloric motlity. Inhibition of endogenous NO synthase with L-Nitro Arginine Methyl Ester (L-NAME, 100 mg kg-1 close i.a.) caused a marked increase of phase pyloric motor activity from 349 +/- 59 to 1044 +/- 140 mmHg min-1 (P < 0.01). In addition, SNAP caused marked stimulation of pyloric tone from 2.6 +/- 0.5 to 13.1 +/- 2.8 mmHg (P < 0.01). Central nervous administration of L-NAME caused modest enhancement of phasic pyloric activity (248 +/- 31 to 283 +/- 32 mmHg min-1 P < 0.05) and pyloric tone (2.6 +/- 0.5 to 3.7 +/- 0.7 mmHg, P < 0.05). Our data indicate that motor activity of the ferret pylorus is potently modulated by NO released within the upper gut. Additionally, there is potential for modulation of pyloric motility by central nervous system production of NO.

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Gastro-oesophageal afferent and serotonergic inputs to vagal efferent neurones

Cited by 10 publications

References 22 publications

Chemical coding and central projections of gastric vagal afferent neurons

Chemical coding and central projections of gastric vagal afferent neurons

New insights into the treatment of gastroesophageal reflux disease

Pyloric motor response to central and peripheral nitric oxide in the ferret

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