Localization of neurokinin 1 receptor (NK1R) immunoreactivity in rat esophagus

Kuramoto, Hirofumi; Oomori, Yukio; Murabayashi, Hiroshi; Kadowaki, Makoto; Karaki, Shin-ichiro; Kuwahara, Atsukazu

doi:10.1002/cne.20169

Cited by 13 publications

(15 citation statements)

References 43 publications

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“…The antiserum recognizes a single band of approximately 68-70 kDa molecular weight on western blots of mouse brain (Chemicon datasheet), and has been used by others to stain the cholinergic terminals and neurons of the myenteric plexus in rats and guinea pigs (Mawe et al, 1996; Schicho et al, 2001; Miampamba et al, 2002; Kuramoto et al, 2004; 2006). ChAT is commonly used for detecting parasympathetic cholinergic preganglionic terminals as well as a subset of postganglionic myenteric neurons (Mawe et al, 1996; Mann et al, 1999; Schicho et al, 2001; Miampamba et al, 2002; Kuramoto et al, 2004; 2006). In our samples, the antiserum produced a staining pattern identical to previous reports (Mawe et al, 1996; Mann et al, 1999; Schicho et al, 2001; Miampamba et al, 2002; Kuramoto et al, 2004; 2006).…”

Section: Methodsmentioning

confidence: 99%

“…ChAT is commonly used for detecting parasympathetic cholinergic preganglionic terminals as well as a subset of postganglionic myenteric neurons (Mawe et al, 1996; Mann et al, 1999; Schicho et al, 2001; Miampamba et al, 2002; Kuramoto et al, 2004; 2006). In our samples, the antiserum produced a staining pattern identical to previous reports (Mawe et al, 1996; Mann et al, 1999; Schicho et al, 2001; Miampamba et al, 2002; Kuramoto et al, 2004; 2006). …”

Section: Methodsmentioning

confidence: 99%

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Melanocortin‐4 receptor expression in a vago‐vagal circuitry involved in postprandial functions

Gautron¹,

Lee²,

Funahashi³

et al. 2009

J of Comparative Neurology

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Vagal afferents regulate energy balance by providing a link between the brain and postprandial signals originating from the gut. In the current study, we investigated melanocortin-4 receptor (MC4R) expression in the nodose ganglion, where the cell bodies of vagal sensory afferents reside. Using a line of mice expressing Green Fluorescent Protein (GFP) under the control of the MC4R promoter, we found GFP expression in approximately one third of nodose ganglion neurons. Using immunohistochemistry combined with in situ hybridization, we also demonstrated that ∼20% of GFP-positive neurons coexpressed cholecystokinin receptor A. In addition, we found that the GFP is transported to peripheral tissues by both vagal sensory afferents and motor efferents, which allowed us to assess the sites innervated by MC4R-GFP neurons. GFP-positive efferents that co-expressed choline acetyltransferase specifically terminated in the hepatic artery and the myenteric plexus of the stomach and duodenum. In contrast, GFP-positive afferents that did not express cholinergic or sympathetic markers terminated in the submucosal plexus and mucosa of the duodenum. Retrograde tracing experiments confirmed the innervation of the duodenum by GFP-positive neurons located in the nodose ganglion. Our findings support the hypothesis that MC4R signaling in vagal afferents may modulate the activity of fibers sensitive to satiety signals such as cholecystokinin, and that MC4R signaling in vagal efferents may contribute to the control of the liver and gastrointestinal tract.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Melanocortin‐4 receptor expression in a vago‐vagal circuitry involved in postprandial functions

Gautron¹,

Lee²,

Funahashi³

et al. 2009

J of Comparative Neurology

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“…Since vagal primary afferent fibers (Berthoud et al, 1997) and at least the majority of enteric neurons in the rat esophagus are capsaicinresistant, the most likely source for the capsaicin-sensitive nerve fibers are spinal ganglia (Holzer, 1988). Spinal primary afferents from esophagus and gastrointestinal tract typically coexpress SP, NKA, and CGRP (for references see Rodrigo et al, 1985;Holzer, 1988;Holzer and Holzer-Petsche, 1997a, b;Dü tsch et al, 1998;Kuramoto et al, 2004). Tachykinins and CGRP released from primary afferents mediate their ''local effector'' function (Holzer, 1988).…”

Section: Functional Considerationsmentioning

confidence: 99%

“…Tachykinins and CGRP released from primary afferents mediate their ''local effector'' function (Holzer, 1988). Spinal afferent nerve fibers were shown to closely contact myenteric neurons in the esophagus (Mazzia and Clerc, 1997), and myenteric neurons in the esophagus express NKA receptors (Kuramoto et al, 2004). Thus, key elements of a local reflex arc from capsaicin-sensitive afferents via nitrergic myenteric neurons to motor endplates are present in the esophagus.…”

Section: Functional Considerationsmentioning

confidence: 99%

Enteric co-innervation of motor endplates in the esophagus: state of the art ten years after

Wörl

Neuhuber

2005

Histochem Cell Biol

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The existence of a distinct ganglionated myenteric plexus between the two layers of the striated tunica muscularis of the mammalian esophagus represented an enigma for quite a while. Although an enteric co-innervation of vagally innervated motor endplates in the esophagus has been repeatedly suggested, it was not possible until recently to demonstrate this dual innervation. Ten years ago, we were able to demonstrate that motor endplates in the rat esophagus receive a dual innervation from both vagal nerve fibers originating in the brain stem and from varicose enteric nerve fibers originating in the myenteric plexus. Since then, a considerable amount of data could be raised on enteric co-innervation and its occurrence in a variety of species, including humans, its neurochemistry, spatial relationships on motor endplates, ontogeny, and possible roles during esophageal peristalsis. These data underline the significance of this newly discovered innervation component, although its function is still largely unknown. The aim of this review is to summarize current knowledge about enteric co-innervation of esophageal striated muscle and to provide some hints as to its functional significance.

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“…In these models, the capsaicin‐triggered inhibition of vagally induced striated muscle contractions was significantly, though not completely, reduced by the NOS blocker N G‐nitro‐ l ‐arginine methyl ester (l ‐NAME) and in preparations pretreated with tachykinin receptor antagonists, and was abrogated in neonatally capsaicin‐treated animals 5–7 . This indicated that capsaicin stimulated transient receptor potential vanilloid type 1 (TRPV1) expressing tachykininergic neurons, most likely primary afferents, that in turn excited nitric oxide (NO) releasing co‐innervating neurons via neurokinin‐1 (NK‐1) receptors 8 . The incomplete reduction of the capsaicin‐triggered inhibition by l ‐NAME suggested involvement of synergistic co‐transmitters, e.g.…”

Section: Introductionmentioning

confidence: 99%

Galanin modulates vagally induced contractions in the mouse oesophagus

Boudaka

Wörl

Shiina

et al. 2009

Neurogastroenterology Motil

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Nitrergic myenteric neurons co-innervating motor endplates were previously shown to inhibit vagally induced contractions of striated muscle in the rodent oesophagus. Immunohistochemical demonstration of putative co-transmitters, e.g. galanin, in enteric neurons prompted us to study a possible role of galanin in modulating vagally mediated contractions in an in vitro vagus nerve-oesophagus preparation of the mouse. Galanin (1-16) (1-100 nmol L(-1)), in the presence of the peptidase inhibitor, phenanthroline monohydrate, inhibited vagally induced contractions in a concentration-dependent manner (control: 100%; galanin 1 nmol L(-1): 95.6 +/- 1.6%; galanin 10 nmol L(-1): 57.3 +/- 6.5%; galanin 100 nmol L(-1): 31.2 +/- 8.1%, n = 5). The non-selective galanin receptor antagonist, galantide (100 nmol L(-1)), blocked the inhibitory effect of galanin (10 nmol L(-1)) while the selective non-galanin receptor 1 and galanin receptor 3 antagonists, M871 (1 micromol L(-1)) and SNAP37889 (100 nmol L(-1)), respectively, and the nitric oxide synthase inhibitor, NG-nitro-l-arginine methyl ester (L-NAME) (200 micromol L(-1)), failed to affect this galanin-induced response. Simultaneous application of galantide (100 nmol L(-1)) and L-NAME (200 micromol L(-1)) significantly reduced the inhibitory effect of capsaicin (30 mumol L(-1)) on vagally induced contractions when compared with its effect in the presence of L-NAME alone or in combination with the selective galanin receptor 2 or 3 antagonists. An inhibitory effect of piperine on vagally induced contractions was reduced neither by galantide nor by L-NAME. Immunohistochemistry revealed galanin immunoreactive myenteric neurons and nerve fibres intermingling with cholinergic vagal terminals at motor endplates. These data suggest that galanin from co-innervating enteric neurons co-operates with nitric oxide in modulating vagally induced contractions in the mouse oesophagus.

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Localization of neurokinin 1 receptor (NK1R) immunoreactivity in rat esophagus

Cited by 13 publications

References 43 publications

Melanocortin‐4 receptor expression in a vago‐vagal circuitry involved in postprandial functions

Melanocortin‐4 receptor expression in a vago‐vagal circuitry involved in postprandial functions

Enteric co-innervation of motor endplates in the esophagus: state of the art ten years after

Galanin modulates vagally induced contractions in the mouse oesophagus

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