Distribution of galanin-immunoreactive nerves in the canine gastrointestinal tract

doi:10.1016/0196-9781(94)00170-7

Peptides

Volume 16, Issue 2, 1995, Pages 237-247

https://doi.org/10.1016/0196-9781(94)00170-7 Get rights and content

Abstract

The distribution of nerves containing galanin immunoreactivity (GAL-IR) in the canine gastrointestinal tract was determined by immunohistochemistry. GAL-IR was observed in nerve cell bodies and nerve fibers in all layers of the lower esophagus, gastric antrum, pylorus, ileum, and colon, and in the sphincters of lower esophagus and pylorus. There were numerous GAL-IR-containing nerve cell bodies in the myenteric plexus of gastric antrum. GAL-IR nerve somata were also common in the myenteric plexus of lower esophagus, ileum, pylorus, and colon, and in the submucous plexus of stomach, ileum, and colon. GAL-IR-positive nerve fibers were also observed around submucous blood vessels of the stomach. GAL-IR nerves are distributed more widely in the canine enteric nervous system than previously recognized.

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Cited by (23)

Galanin and its receptors: A novel strategy for appetite control and obesity therapy
2012, Peptides
Citation Excerpt :
Several food intake regulatory peptides, including galanin, also influence gastrointestinal motility and function. In the gastrointestinal tract, galanin immunoreactivity is expressed by enteric neurons localized in the submucous and myenteric plexus, and its fibers project to the gut wall [36,44,130]. The effects of galanin on gastrointestinal motility are both stimulatory and inhibitory, depending on different tissues, species and experimental conditions [40,65,91,121].
The rapid increase in the prevalence of overweight and obesity is becoming an important health problem. Overweight and obesity may cause several metabolic complications, including type 2 diabetes mellitus, hyperlipidemia, high cholesterol, coronary artery disease as well as hypertension. Prevention and treatment of obesity will benefit the treatment of these related diseases. Current strategies for treatment of obesity are not adequately effective and are frequently companied with many side effects. Thus, new ways to treat obesity are urgently needed. Galanin is undoubtedly involved in the regulation of food intake and body weight. The aim of this review is to provide up-to-date knowledge concerning the roles of central and peripheral galanin as well as its receptors in the regulation of metabolism, obesity and appetite. We also highlight the mechanisms of galanin and its receptors in experimental obesity, trying to establish a novel anti-obesity strategy.
The galanin peptide family: Receptor pharmacology, pleiotropic biological actions, and implications in health and disease
2007, Pharmacology and Therapeutics
The galanin peptide family consists of the “parental” galanin, galanin-message-associated peptide (GMAP) which derives from the same peptide precursor gene product as galanin, galanin-like peptide (GALP) encoded by a different gene, and the recently discovered peptide alarin which is encoded by a splice variant of the GALP gene. The galanin receptor family currently comprises 3 members, GalR1, GalR2, and GalR3, which are all G-protein-coupled receptors. This review will provide an overview of the comprehensive, pharmacological characterization of endogenous and synthetic galanin receptor ligands and their interactions with the galanin receptors, a summary of the various (pleiotropic) biological actions of galanin and GALP (and alarin), and briefly discuss the implications of pathological changes for health and disease and potential clinical therapeutics. Since its discovery more than 20 years ago, a large number of putative physiological functions have been ascribed to galanin, and active research still continues to validate these functions and determine their importance for physiology and pathology. Since the more recent identification of GALP, considerable research has identified functions for this peptide in the central nervous system (CNS), but the identity of its preferred, native receptor is still unknown. Little is known of the role of alarin apart from evidence of its expression and a vasoactive action in the skin. The wide range of functions of the galanin peptide family indicates an essential role for galanin signaling in “mind and body homeostasis” and a potential therapeutic efficacy in a variety of human diseases, particularly epilepsy, Alzheimer's disease, and diabetes.
Expression of galanin receptor messenger RNAs in different regions of the rat gastrointestinal tract
2005, Peptides
Galanin effects are mediated by three G-protein-coupled receptors: galanin receptor 1 (GalR1), GalR2 and GalR3. We quantified mRNA levels of GalR1, GalR2 and GalR3 in the rat stomach, small and large intestine using real-time RT-PCR. All three GalR mRNAs were detected throughout the gut at different levels. GalR1 and GalR2 mRNA levels were higher in the large than in the small intestine. GalR2 mRNA was most abundant in the stomach. GalR3 mRNA levels were generally quite low. The differential regional distribution of GalRs suggests that the complex effects of galanin in the gut are the result of activating multiple receptor subtypes, whose density, subtype and signaling vary along the gastrointestinal tract.
Galanin inhibits gastric acid secretion through a somatostatin-independent mechanism in mice
2004, Peptides
The role of somatostatin in galanin-induced inhibition of gastric acid secretion in urethane-anesthetized mice was investigated by using immunoneutralization of endogenous somatostatin and somatostatin receptor type 2 (SSTR2) knockout mice. Intravenous galanin (10 and 20 μg/kg/h) inhibited pentagastrin-stimulated gastric acid secretion by 47 and 33%, respectively. Somatostatin antibody injected i.v. increased acid secretion by 3.5-fold over basal levels but did not modify the antisecretory effects of galanin. Urethane-anesthetized SSTR2 knockout mice had a basal secretion 14-fold higher than wild-type animals, that was inhibited by galanin (10 and 20 μg/kg/h) by 49 and 31% respectively. In mice galanin inhibits gastric acid secretion through a somatostatin-independent mechanism.
Colocalization of inhibitory mediators, NO, VIP and galanin, in canine enteric nerves
1998, Peptides
Wang, Y. F., Y. K. Mao, J. E. T. Fox–threlkeld, T. J. McDonald and E. E. Daniel. Colocalization of inhibitory mediators, NO, VIP and Galanin, in canine enteric nerves. Peptides 19(1), 99–112, 1998.—The colocalization of three putative inhibitory mediators of enteric nerves, vasoactive intestinal peptide (VIP), galanin (GAL) and nitric oxide synthase (nNOS), was examined in the myenteric plexus of canine antrum, intestine and colon. Many ileal and colonic neurons contained nNOS-immunoreactive (nNOS-IR) activity with some also containing VIP-IR; only a few neurons also contained GAL-IR. Ileal and colonic VIP-IR nerves often appeared to be interneurons innervating nNOS nerves. Many antral neurons contained VIP-IR with nearly all also containing GAL-IR. A few also contained nNOS-IR. The predominance of nNOS-IR neurons relative to VIP-IR and GAL-IR neurons in the ileal and colonic, but not the antral, myenteric plexus is consistent with NO being the primary inhibitory mediator in the intestine but not in the antrum.
Galanin inhibition of Enterochromaffin-like cell function
1998, Gastroenterology
Background & Aims: Galanin, a 29–amino acid neuropeptide found in the gastric mucosa, inhibits basal and pentagastrin-stimulated acid secretion. Its cellular target is unknown. The aim of this study was to determine whether galanin inhibits Ca²⁺ signaling and histamine release in enterochromaffin-like (ECL) cells. Methods: Isolated rat ECL cells were purified to 85% homogeneity by a combination of elutriation, density gradient centrifugation, and 48-hour culture. Intracellular calcium concentration ([Ca²⁺]_i) was determined using video imaging with Fura-2 in a 37°C superfusion chamber. Histamine was measured by radioimmunoassay. Results: Reverse-transciption polymerase chain reaction of the ECL cell RNA showed a galanin type I receptor subtype. Galanin inhibited gastrin, Bay K8644, and K⁺ depolarization–induced calcium mobilization and entry as well as reduced basal calcium levels. Pretreatment with pertussis toxin decreased the effect of galanin. Galanin inhibited basal and gastrin-stimulated histamine release by approximately 60% with a median effective concentration of 1.10⁻¹⁰ mol/L. The inhibitory actions of galanin on histamine release and Ca²⁺ influx could be reduced by a galanin antagonist, galantide. Conclusions: Galanin's inhibition of acid secretion can be explained in part by inhibition of calcium signaling and histamine release from the ECL cells due to activation of a G_i,o protein–coupled receptor.
GASTROENTEROLOGY 1998;115:330-339

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ArticleDistribution of galanin-immunoreactive nerves in the canine gastrointestinal tract

Abstract

Life Sci.

Regul. Pept.

Life Sci.

Eur. J. Pharmacol.

FEBS Lett.

Gastroenterology

Inhibitory function of VIP, PHI and galanin in canine pylorus

Am. J. Physiol.

Characterization of galanin receptor in canine small intestinal circular muscle synaptosomes

Am. J. Physiol. Gastrointest. Liver Physiol.

Article
Distribution of galanin-immunoreactive nerves in the canine gastrointestinal tract