neuropeptide-y and Megacolon

neuropeptide-y has been researched along with Megacolon* in 2 studies

Other Studies

2 other study(ies) available for neuropeptide-y and Megacolon

Article	Year
A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice. The Journal of clinical investigation, 1997, Aug-15, Volume: 100, Issue:4 The Ncx/Hox11L.1 gene, a member of the Hox11 homeobox gene family, is mainly expressed in neural crest-derived tissues. To elucidate the role of Ncx/Hox11L.1, the gene has been inactivated in embryonic stem cells by homologous recombination. The homozygous mutant mice were viable. These mice developed megacolon with enteric ganglia by age 3-5 wk. Histochemical analysis of the ganglia revealed that the enteric neurons hyperinnervated in the narrow segment of megacolon. Some of these neuronal cells degenerated and neuronal cell death occurred in later stages. We propose that Ncx/Hox11L.1 is required for maintenance of proper functions of the enteric nervous system. These mutant mice can be used to elucidate a novel pathogenesis for human neuronal intestinal dysplasia. Topics: Animals; Colon; Enteric Nervous System; Ganglia; Homeodomain Proteins; Immunohistochemistry; Megacolon; Mice; Mice, Knockout; NADPH Dehydrogenase; Neuropeptide Y; Oncogene Proteins; Substance P	1997
Megacolon in myotonic dystrophy caused by a degenerative neuropathy of the myenteric plexus. Gastroenterology, 1988, Volume: 95, Issue:3 A 32-yr-old man with myotonic dystrophy had a left hemicolectomy performed because of a megacolon. The colonic mucosa, smooth muscle, and connective tissue appeared normal by hematoxylin and eosin and trichrome stains and transmission electron microscopy. In contrast, the myenteric plexus had markedly fewer neurons than normal on the hematoxylin and eosin stains. Silver staining of the plexus revealed degeneration and decreased numbers of argyrophilic neurons, which were smaller and had fewer processes and a more uneven staining quality than controls. Many axons were fragmented, and increased numbers of glial cell nuclei were present in the plexus. Degenerative changes in the neurons were present in a patchy distribution on transmission electron microscopy. Immunohistochemistry revealed a decrease of the substance P- and enkephalin-immunoreactive fibers in the muscularis externa. This suggests that colonic motor dysfunction associated with myotonic dystrophy may be caused by a visceral neuropathy that involves the substance P- and enkephalin-immunoreactive fibers of the smooth muscle. Topics: Adult; Colon; Enkephalins; Histocytochemistry; Humans; Male; Megacolon; Myenteric Plexus; Myotonic Dystrophy; Nerve Degeneration; Nerve Fibers; Neuropeptide Y; Radiography; Substance P; Vasoactive Intestinal Peptide	1988

Article

Year

A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice.

The Journal of clinical investigation, 1997, Aug-15, Volume: 100, Issue:4

The Ncx/Hox11L.1 gene, a member of the Hox11 homeobox gene family, is mainly expressed in neural crest-derived tissues. To elucidate the role of Ncx/Hox11L.1, the gene has been inactivated in embryonic stem cells by homologous recombination. The homozygous mutant mice were viable. These mice developed megacolon with enteric ganglia by age 3-5 wk. Histochemical analysis of the ganglia revealed that the enteric neurons hyperinnervated in the narrow segment of megacolon. Some of these neuronal cells degenerated and neuronal cell death occurred in later stages. We propose that Ncx/Hox11L.1 is required for maintenance of proper functions of the enteric nervous system. These mutant mice can be used to elucidate a novel pathogenesis for human neuronal intestinal dysplasia.

Topics: Animals; Colon; Enteric Nervous System; Ganglia; Homeodomain Proteins; Immunohistochemistry; Megacolon; Mice; Mice, Knockout; NADPH Dehydrogenase; Neuropeptide Y; Oncogene Proteins; Substance P

1997

Megacolon in myotonic dystrophy caused by a degenerative neuropathy of the myenteric plexus.

Gastroenterology, 1988, Volume: 95, Issue:3

A 32-yr-old man with myotonic dystrophy had a left hemicolectomy performed because of a megacolon. The colonic mucosa, smooth muscle, and connective tissue appeared normal by hematoxylin and eosin and trichrome stains and transmission electron microscopy. In contrast, the myenteric plexus had markedly fewer neurons than normal on the hematoxylin and eosin stains. Silver staining of the plexus revealed degeneration and decreased numbers of argyrophilic neurons, which were smaller and had fewer processes and a more uneven staining quality than controls. Many axons were fragmented, and increased numbers of glial cell nuclei were present in the plexus. Degenerative changes in the neurons were present in a patchy distribution on transmission electron microscopy. Immunohistochemistry revealed a decrease of the substance P- and enkephalin-immunoreactive fibers in the muscularis externa. This suggests that colonic motor dysfunction associated with myotonic dystrophy may be caused by a visceral neuropathy that involves the substance P- and enkephalin-immunoreactive fibers of the smooth muscle.

Topics: Adult; Colon; Enkephalins; Histocytochemistry; Humans; Male; Megacolon; Myenteric Plexus; Myotonic Dystrophy; Nerve Degeneration; Nerve Fibers; Neuropeptide Y; Radiography; Substance P; Vasoactive Intestinal Peptide

1988