Abdominal Vagotomy Blocks the Satiety Effect of Cholecystokinin in the Rat

Smith, G.P.; Jerome, C.; Cushin, BJ; Eterno, R; Simansky, Kenny J.

doi:10.1126/science.7268408

Cited by 754 publications

(225 citation statements)

References 10 publications

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“…The satiety-inducing effects of CCK require an intact vagus nerve. 57 CCK excites vagal afferent fibres with mucosal endings, 58 and both long chain fatty acids and casein cause activation of vagal mucosal afferents, which is blocked by CCK A antagonists. 59,60 PYY also excites vagal afferent neurons and its satiety-mediating effects might require intact vagal nerve connections, 61,62 although it also acts hormonally in the brain.…”

Section: Vagal Mucosal Afferentsmentioning

confidence: 99%

Extrinsic primary afferent signalling in the gut

Brookes

Spencer

Costa

et al. 2013

Nat Rev Gastroenterol Hepatol

246

216

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Visceral sensory neurons activate reflex pathways that control gut function and also give rise to important sensations, such as fullness, bloating, nausea, discomfort, urgency and pain. Sensory neurons are organised into three distinct anatomical pathways to the central nervous system (vagal, thoracolumbar and lumbosacral). Although remarkable progress has been made in characterizing the roles of many ion channels, receptors, and second messengers in visceral sensory neurons, the basic aim of understanding how many classes there are, and how they differ, has proven difficult to achieve. We suggest that there are just five structurally distinct types of sensory endings in the gut wall that account for essentially all of the primary afferent neurons in the three pathways. Each of these five major structural types of endings seems to show distinctive combinations of physiological responses. These types are: 'intraganglionic laminar' endings in myenteric ganglia; 'mucosal' endings located in the subepithelial layer; 'muscular mucosal' afferents, with mechanosensitive endings close to the muscularis mucosae; 'intramuscular' endings, with endings within the smooth muscle layers; and 'vascular' afferents, with sensitive endings primarily on blood vessels. 'Silent' afferents might be a subset of inexcitable 'vascular' afferents, which can be switched on by inflammatory mediators.Extrinsic sensory neurons comprise an attractive focus for targeted therapeutic intervention in a range of gastrointestinal disorders.2

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Section: Vagal Mucosal Afferentsmentioning

confidence: 99%

Extrinsic primary afferent signalling in the gut

Brookes

Spencer

Costa

et al. 2013

Nat Rev Gastroenterol Hepatol

246

216

View full text Add to dashboard Cite

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“…The satiation effects of CCK must be strengthened by the following two pathways to the hindbrain: regulation of the nucleus tractus solitarium (NTS) via vagal afferents (Raybould et al 1988;Smith et al 1981;, and hormonal regulation of the area postrema, another center of feeding behavior with a leaky blood-brain barrier in the hindbrain (Glatzle et al 2001;Ladenheim et al 1988;Moran et al 1990). CCK1 receptor-immunoreactive nerve fibers were found in the present study to be absent in the mucosal layer but gather in the myenteric nerve plexus of the antro-duodenum; they may be projected to the hindbrain via the nodose ganglia.…”

Section: Cck1 Receptors In the Antro-duodenal Regionmentioning

confidence: 99%

Cellular and subcellular localization of cholecystokinin (CCK)-1 receptors in the pancreas, gallbladder, and stomach of mice

Konno

Takahashi-Iwanaga

Uchigashima

et al. 2014

Histochem Cell Biol

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“…After a midline incision of the abdominal wall, the lower part of the esophagus was exposed and the anterior and posterior branches of the vagal nerve were incised under anesthesia with sodium pentobarbital (50 mg/kg of body weight, i.p. ), as previously described (Smith et al 1981). During the sham operations, the vagal trunks were similarly exposed without any cutting of the vagal nerve.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

Mano-Otagiri¹,

Ohata²,

Iwasaki-Sekino³

et al. 2009

Journal of Endocrinology

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To clarify the role of ghrelin in the regulatory mechanism of energy metabolism, we analyzed the effects of centrally and peripherally administered ghrelin on noradrenaline release in the brown adipose tissue (BAT) of rats using a microdialysis system. I.c.v. administration of ghrelin at a dose of 500 pmol suppressed noradrenaline release in BAT, and microinjection of ghrelin (50 pmol) into the paraventricular nucleus (PVN) or arcuate nucleus (ARC) of the hypothalamus also suppressed noradrenaline release in BAT. In addition, i.v. administered ghrelin (30 nmol) suppressed noradrenaline release in BAT, and this suppression was blocked by a vagotomy. Neither i.c.v. nor i.v. administration of des-acyl ghrelin, which does not bind to GH secretagogue receptor type 1a (GHS-R1a), affected noradrenaline release in BAT. These results indicate that ghrelin increases energy storage by suppressing the activity of the sympathetic nerve innervating BAT. It seems that the PVN and ARC, which express GHSR1a, are the sites of action of ghrelin in the brain and that the action of peripheral ghrelin on the sympathetic nerve activity innervating BAT is mediated by the vagal nerve, which also expresses GHS-R1a.

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Abdominal Vagotomy Blocks the Satiety Effect of Cholecystokinin in the Rat

Cited by 754 publications

References 10 publications

Extrinsic primary afferent signalling in the gut

Extrinsic primary afferent signalling in the gut

Cellular and subcellular localization of cholecystokinin (CCK)-1 receptors in the pancreas, gallbladder, and stomach of mice

Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

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