Peptide YY receptor in submucosal and myenteric plexus synaptosomes of canine small intestine

Mao, Yu; Wang, Y. F.; Ward, G. R.; Cipris, S.; Daniel, E. E.; McDonald, Thomas J.

doi:10.1152/ajpgi.1996.271.1.g36

Cited by 14 publications

(13 citation statements)

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“…The presence of Y1-R in the colon was confirmed by identification of a Y1-R-specific protein of 70 kD, corresponding to the previous published size of Y1-R (Sheikh and Williams 1990;Inui et al 1992;Mao et al 1996). Throughout the rat intestine, specific Y1-R immunoreactivity could be localized to many nerve cell bodies of the submucosal and myenteric plexi.…”

Section: Discussionsupporting

confidence: 57%

“…Throughout the rat intestine, specific Y1-R immunoreactivity could be localized to many nerve cell bodies of the submucosal and myenteric plexi. Previous studies have also demonstrated the presence of NPY/PYY binding sites in submucosal and myenteric neurons by receptor autoradiography (Walsh et al 1993;Mao et al 1996). These studies, however, were not able to differentiate between NPY/PYY receptor subtypes.…”

Section: Discussionmentioning

confidence: 88%

“…Earlier studies have localized NPY and PYY binding sites to submucosal and myenteric plexi in the gastrointestinal tract using receptor autoradiography (Walsh et al 1993;Mao et al 1996). The identity of these binding sites was further analyzed using the NPY analogues [Leu 31 , Pro 34 ]-NPY and NPY , which preferentially bind to the Y1-R and the Y2 receptor, respectively.…”

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confidence: 99%

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Immunocytochemical Localization of the NPY/PYY Y1 Receptor in Enteric Neurons, Endothelial Cells, and Endocrine-like Cells of the Rat Intestinal Tract

Jackerott

Larsson

1997

J Histochem Cytochem.

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SUMMARY Neuropeptide Y (NPY) and peptide YY (PYY) are structurally related peptides that are considered to mediate inhibitory actions on gastrointestinal motility, secretion, and blood flow. Several receptor subtypes for these peptides have been identified and the Y1, Y2, Y4/PP1, Y5, and Y5/PP2/Y2b receptors have been cloned. In this article we report the immunocytochemical localization of the Y1 receptor to myenteric and submucosal nerve cell bodies, endothelial cells, and scattered endocrine-like cells of rat intestinal tract. Moreover, double immunofluorescence demonstrates that subpopulations of the Y1 receptorpositive nerve cell bodies are immunopositive for NPY, vasoactive intestinal polypeptide, and nitric oxide synthase. In part, such co-localizations were made possible by use of peroxidase-mediated deposition of tyramide, which permitted use of antisera derived from the same species. Our observations suggest the existence of multiple neuronal, endothelial, and endocrine target sites for NPY and PYY and that some of the actions of these regulatory peptides can be mediated by vasoactive intestinal peptide and nitric oxide synthase.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

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Immunocytochemical Localization of the NPY/PYY Y1 Receptor in Enteric Neurons, Endothelial Cells, and Endocrine-like Cells of the Rat Intestinal Tract

Jackerott

Larsson

1997

J Histochem Cytochem.

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“…NPY and PYY bind to and activate receptors Y 1 , Y 2 , and Y 5 , and PP binds to receptor Y 4 (Cox et al 2001;Cox and Tough 2002;Hyland and Cox 2005;Hyland et al 2003). Receptors Y 1 , Y 2 , and Y 4 have been found in the colon and small intestine, localized to epithelial cells and neurons belonging to the submucosal and myenteric plexus (Cox et al 2001;Cox and Tough 2002;Gregor et al 1996a;Gregor et al 1996b;Gue et al 1996;Inui et al 1992;Mao et al 1996;Sheikh and Williams 1990;Walsh et al 1993;Wharton et al 1993;Yan et al 1996).…”

Section: The Npy Family Of Peptidesmentioning

confidence: 99%

The role of the neuropeptide Y (NPY) family in the pathophysiology of inflammatory bowel disease (IBD)

Hausken

2016

Neuropeptides

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Inflammatory bowel disease (IBD) includes three main disorders: ulcerative colitis, Crohn's disease, and microscopic colitis. The etiology of IBD is unknown and the current treatments are not completely satisfactory. Interactions between the gut neurohormones and the immune system are thought to play a pivot role in inflammation, especially in IBD. These neurohormones are believed to include members of the neuropeptide YY (NPY) family, which comprises NPY, peptide YY (PYY), and pancreatic polypeptide (PP). Understanding the role of these peptides may shed light on the pathophysiology of IBD and potentially yield an effective treatment tool. Intestinal NPY, PYY, and PP are abnormal in both patients with IBD and animal models of human IBD. The abnormality in NPY appears to be primarily caused by an interaction between immune cells and the NPY neurons in the enteric nervous system; the abnormalities in PYY and PP appear to be secondary to the changes caused by the abnormalities in other gut neurohormonal peptides/amines that occur during inflammation. NPY is the member of the NPY family that can be targeted in order to decrease the inflammation present in IBD.

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“…NPY-immunoreactive nerve fibers are abundant in GI tract (22,23). With the use of receptor autoradiography, NPY and peptide YY (PYY) binding sites have been localized to submucosal and myenteric plexi (30,45). In the GI tract, NPY and PYY have been shown to be potent inhibitors of intestinal fluid, electrolyte secretion, and motility (36, 38).…”

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confidence: 99%

Attenuation of acute experimental colitis by preventing NPY Y1 receptor signaling

Hassani

Lucas

Rozell

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Neuropeptide Y (NPY), a 36-amino acid peptide, is widely expressed in the central and peripheral nervous system. NPY is involved in the regulation of several physiological processes, including energy balance, food intake, and nociception. Recently, we showed that activation of the NPY Y1 receptor is required for cutaneous neurogenic inflammation. Because neurogenic inflammation could participate in colitis, the aim of this study was to investigate the role of the NPY Y1 receptor in acute colitis using mice genetically deficient of NPY Y1 receptor. In addition, the Y1 receptor antagonist H409/22, was also investigated. Animals received 5% dextran sulfate sodium (DSS) in drinking water for 7 days. One group of animals also received the Y1 receptor antagonist, administered intraperitoneally twice daily. Disease activity was assessed daily for 7 days in all groups. DSS induced colitis in all animals resulting in weight loss, diarrhea, epithelial damage, crypt shortening, and inflammatory infiltration. However, clinical manifestation of the disease was markedly attenuated in Y1 null mutant mice as well as in mice receiving the Y1 antagonist. Histological analysis showed that tissue damage and ulceration were less severe in Y1-deficient animals. Consistent with the clinical and histological data, capsaicin-induced plasma extravasation was significantly reduced in the gut of Y1 null mutant animals compared with treated wild-type animals. These data indicate that NPY and Y1 receptor are involved in intestinal inflammation and suggest that inhibition of NPY Y1 receptor signaling may provide a novel therapeutic approach in the treatment of colonic inflammation. neurogenic inflammation; dextran sulfate sodium; in vivo animal models ULCERATIVE COLITIS AND CROHN'S disease constitute the two main forms of inflammatory bowel disease (IBD). This disease is characterized by a dysregulated immune response and chronic relapsing inflammation of the gastrointestinal (GI) tract, leading to diarrhea, hemoccult, abdominal pain, weight loss, and anemia.Despite intense research, the etiology of IBDs remains largely unknown. The development of IBD involves interactions among genetic, immunological, and environmental components (46). Other mediators implicated in the pathogenesis of colitis are neuropeptides released from enteric and sensory afferent neurons (37). These peptides have been shown to modulate different aspects of mucosal function, including blood flow and secretion, and may play a role in the recruitment of granulocytes and lymphocytes and in the modulation of mast cell activation (14,18).Stimulation and activation of capsaicin-sensitive sensory nerve endings produce an inflammatory response characterized by vasodilation and plasma extravasation (13). The inflammatory response is mediated by local release of sensory neuropeptides such as substance P (SP) and calcitonin gene-related peptide (CGRP) (25). The inflammatory response, termed neurogenic inflammation, is well described in many peripheral organs including the skin, ai...

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Peptide YY receptor in submucosal and myenteric plexus synaptosomes of canine small intestine

Cited by 14 publications

References 0 publications

Immunocytochemical Localization of the NPY/PYY Y1 Receptor in Enteric Neurons, Endothelial Cells, and Endocrine-like Cells of the Rat Intestinal Tract

Immunocytochemical Localization of the NPY/PYY Y1 Receptor in Enteric Neurons, Endothelial Cells, and Endocrine-like Cells of the Rat Intestinal Tract

The role of the neuropeptide Y (NPY) family in the pathophysiology of inflammatory bowel disease (IBD)

Attenuation of acute experimental colitis by preventing NPY Y1 receptor signaling

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