Galanin is Co-Expressed with Substance P, Calbindin and Corticotropin-Releasing Factor (CRF) in The Enteric Nervous System of the Wild Boar (Sus scrofa) Small Intestine

2015 ◽  
Vol 45 (2) ◽  
pp. 115-123 ◽  
Author(s):  
A. Czujkowska ◽  
M. B. Arciszewski
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Substance P ◽  
Enteric Nervous System ◽  
Wild Boar ◽  
Sus Scrofa ◽  
Corticotropin Releasing Factor

Analysis of the role of 5-HT in the enteric nervous system using anti-idiotopic antibodies to 5-HT receptors

1994 ◽  
Vol 266 (3) ◽  
pp. G403-G416 ◽  
Author(s):  
P. R. Wade ◽  
H. Tamir ◽  
A. L. Kirchgessner ◽  
M. D. Gershon
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Enteric Nervous System ◽  
Binding Sites ◽  
Input Resistance ◽  
Gastrointestinal Function ◽  
Postsynaptic Potentials

The effects of anti-idiotypic antibodies (alpha-id) that recognize serotonin [5-hydroxytryptamine (5-HT)] receptors on myenteric neurons of the guinea pig small intestine were characterized electrophysiologically, and alpha-id binding sites were located immunocytochemically. Initial applications of the alpha-id mimicked each of three actions of 5-HT: a rapid depolarization, associated with a fall in input resistance (Rin), which was inhibited by the 5-HT3 antagonists tropisetron (> or = 1 microM) and renzapride (100 microM); a slow membrane depolarization, associated with increased Rin, that was inhibited by the 5-HT1P antagonist renzapride but was unaffected by a 5-HT4 blocking concentration of tropisetron (10 microM); and a hyperpolarization, associated with decreased Rin, that was antagonized by the 5-HT1A inhibitor NAN-190. Cross-desensitization was observed between responses to 5-HT and the alpha-id. After exposure to the alpha-id, subsequent responses to the alpha-id, 5-HT, and stimulus-evoked slow excitatory postsynaptic potentials were antagonized; however, responses to carbachol and substance P were unaffected. The alpha-id thus specifically inhibits the effects of endogenously released and exogenously applied 5-HT. The alpha-id bound to sites on myenteric and submucosal neurons and a subepithelial nerve plexus. Binding of the alpha-id was blocked by 5-HT1P-, 5-HT3-, and 5-HT4-specific antagonists. We concluded that the alpha-id binds selectively to all known subtypes of 5-HT receptor in the enteric nervous system and is thus useful for investigating the gastrointestinal function of 5-HT.

scholarly journals Dopamine Transporter Genetic Reduction Induces Morpho-Functional Changes in the Enteric Nervous System

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 465
Author(s):  
Silvia Cerantola ◽  
Valentina Caputi ◽  
Gabriella Contarini ◽  
Maddalena Mereu ◽  
Antonella Bertazzo ◽  
...  
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Enteric Nervous System ◽  
Dopamine Transporter ◽  
Myenteric Plexus ◽  
Receptor Activation ◽  
D1 Receptor ◽  
Functional Changes ◽  
Neurochemical Coding ◽  
The Impact

Antidopaminergic gastrointestinal prokinetics are indeed commonly used to treat gastrointestinal motility disorders, although the precise role of dopaminergic transmission in the gut is still unclear. Since dopamine transporter (DAT) is involved in several brain disorders by modulating extracellular dopamine in the central nervous system, this study evaluated the impact of DAT genetic reduction on the morpho-functional integrity of mouse small intestine enteric nervous system (ENS). In DAT heterozygous (DAT+/−) and wild-type (DAT+/+) mice (14 ± 2 weeks) alterations in small intestinal contractility were evaluated by isometrical assessment of neuromuscular responses to receptor and non-receptor-mediated stimuli. Changes in ENS integrity were studied by real-time PCR and confocal immunofluorescence microscopy in longitudinal muscle-myenteric plexus whole-mount preparations (). DAT genetic reduction resulted in a significant increase in dopamine-mediated effects, primarily via D1 receptor activation, as well as in reduced cholinergic response, sustained by tachykininergic and glutamatergic neurotransmission via NMDA receptors. These functional anomalies were associated to architectural changes in the neurochemical coding and S100β immunoreactivity in small intestine myenteric plexus. Our study provides evidence that genetic-driven DAT defective activity determines anomalies in ENS architecture and neurochemical coding together with ileal dysmotility, highlighting the involvement of dopaminergic system in gut disorders, often associated to neurological conditions.

Actions of cysteinyl leukotrienes in the enteric nervous system of guinea-pig stomach and small intestine

2003 ◽  
Vol 459 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Sumei Liu ◽  
Hong-Zhen Hu ◽  
Chuanyun Gao ◽  
Na Gao ◽  
Guodu Wang ◽  
...  
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Guinea Pig ◽  
Enteric Nervous System ◽  
Cysteinyl Leukotrienes ◽  
Guinea Pig Stomach

Substance P and NK1 receptor expression in the enteric nervous system is related to the development of chagasic megacolon

2008 ◽  
Vol 102 (11) ◽  
pp. 1154-1156 ◽  
Author(s):  
Alexandre B.M. da Silveira ◽  
Michelle A.R. Freitas ◽  
Enio C. de Oliveira ◽  
Salustiano G. Neto ◽  
Alejandro O. Luquetti ◽  
...  
Keyword(s):  
Nervous System ◽  
Substance P ◽  
Enteric Nervous System ◽  
Receptor Expression ◽  
Nk1 Receptor ◽  
Chagasic Megacolon

Effects of optogenetic activation of the enteric nervous system on gastrointestinal motility in mouse small intestine

2020 ◽  
Vol 229 ◽  
pp. 102733
Author(s):  
Nick J. Spencer ◽  
Lee Travis ◽  
Tim Hibberd ◽  
Nigel Kelly ◽  
Jing Feng ◽  
...  
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Enteric Nervous System ◽  
Gastrointestinal Motility ◽  
Mouse Small Intestine

P2X7 receptors in the enteric nervous system of guinea-pig small intestine

2001 ◽  
Vol 440 (3) ◽  
pp. 299-310 ◽  
Author(s):  
Hong-Zhen Hu ◽  
Na Gao ◽  
Zhong Lin ◽  
Chuanyun Gao ◽  
Sumei Liu ◽  
...  
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Guinea Pig ◽  
Enteric Nervous System ◽  
P2x7 Receptors

Role of glial cell-line derived neurotropic factor family receptor α2 in the actions of the glucagon-like peptides on the murine intestine

2007 ◽  
Vol 293 (2) ◽  
pp. G461-G468 ◽  
Author(s):  
Sean C. McDonagh ◽  
Jenny Lee ◽  
Angelo Izzo ◽  
Patricia L. Brubaker
Keyword(s):  
Nervous System ◽  
Substance P ◽  
Enteric Nervous System ◽  
Cell Line ◽  
Glial Cell ◽  
Wild Type ◽  
Intestinal Growth ◽  
Mrna Transcripts ◽  
Neurotropic Factor

The intestinal glucagon-like peptides GLP-1 and GLP-2 inhibit intestinal motility, whereas GLP-2 also stimulates growth of the intestinal mucosa. However, the mechanisms of action of these peptides in the intestine remain poorly characterized. To determine the role of the enteric nervous system in the actions of GLP-1 and GLP-2 on the intestine, the glial cell line-derived neurotropic factor family receptor α2 (GFRα2) knockout (KO) mouse was employed. The mice exhibited decreased cholinergic staining, as well as reduced mRNA transcripts for substance P-ergic excitatory motoneurons in the enteric nervous system (ENS) ( P < 0.05). Examination of parameters of intestinal growth (including small and large intestinal weight and small intestinal villus height, crypt depth, and crypt cell proliferation) demonstrated no differences between wild-type and KO mice in either basal or GLP-2-stimulated mucosal growth. Nonetheless, KO mice exhibited reduced numbers of synaptophysin-positive enteroendocrine cells ( P < 0.05), as well as a markedly impaired basal gastrointestinal (GI) transit rate ( P < 0.05). Furthermore, acute administration of GLP-1 and GLP-2 significantly inhibited transit rates in wild-type mice ( P < 0.05–0.01) but had no effect in GFRα2 KO mice. Despite these changes, expression of mRNA transcripts for the GLP receptors was not reduced in the ENS of KO animals, suggesting that GLP-1 and -2 modulate intestinal transit through enhancement of inhibitory input to cholinergic/substance P-ergic excitatory motoneurons. Together, these findings demonstrate a role for GFRα2-expressing enteric neurons in the downstream signaling of the glucagon-like peptides to inhibit GI motility, but not in intestinal growth.

Sign in / Sign up

Export Citation Format

Share Document