The neurohypophysial peptide oxytocin (OT) and OT-like hormones facilitate reproduction in all vertebrates at several levels. The major site of OT gene expression is the magnocellular neurons of the hypothalamic paraventricular and supraoptic nuclei. In response to a variety of stimuli such as suckling, parturition, or certain kinds of stress, the processed OT peptide is released from the posterior pituitary into the systemic circulation. Such stimuli also lead to an intranuclear release of OT. Moreover, oxytocinergic neurons display widespread projections throughout the central nervous system. However, OT is also synthesized in peripheral tissues, e.g., uterus, placenta, amnion, corpus luteum, testis, and heart. The OT receptor is a typical class I G protein-coupled receptor that is primarily coupled via Gq proteins to phospholipase C-β. The high-affinity receptor state requires both Mg2+ and cholesterol, which probably function as allosteric modulators. The agonist-binding region of the receptor has bee...

The Oxytocin Receptor System: Structure, Function, and Regulation

Neuroanatomical Localization, Pharmacological Characterization and Functions of CGRP, Related Peptides and Their Receptors

Calcitonin gene-related peptide: Detailed immunohistochemical distribution in the central nervous system

Calcitonin gene-related peptide coexists with substance P in capsaicin sensitive neurons and sensory ganglia of the rat.

Characterization of the peptidergic afferent innervation of the stomach in the rat, mouse and guinea-pig

Calcitonin gene-related peptide acts within the central nervous system to inhibit gastric acid secretion

https://www.gastrojournal.org/article/0016-5085(86)90693-1/pdf

Inhibition of gastric acid secretion by brain peptides in the dog. Role of the autonomic nervous system and gastrin.

This study was designed to assess the central nervous system actions of human calcitonin (hCalc) and human calcitonin gene-related peptide (hCGRP) on meal-stimulated gastric acid secretion in awake beagle dogs. hCalc (0.1–1.0 nmol/kg) and hCGRP (0.01–1.0 nmol/kg) injected into the third cerebral ventricle significantly inhibited gastric acid secretion stimulated by an 8% peptone meal. hCGRP was ten times more potent than hCalc in inhibiting gastric secretion. Neither hCalc nor hCGRP significantly altered plasma gastrin concentrations compared to control values. Truncal vagotomy did not prevent the gastric inhibitory actions of hCalc and hCGRP. Ganglionic blockade with chlorisondamine completely abolished the gastric inhibitory action of hCalc but had no effect on gastric acid inhibition induced by hCGRP. The results of this study indicate that intracerebroventricular administration of hCalc and hCGRP inhibits meal-stimulated gastric acid secretion in awake dogs. Inhibition of gastric acid secretion by hCalc and hCGRP in the dog is not mediated by inhibition of gastrin release or by the vagus nerves. Human Calc but not human CGRP appears to inhibit meal-stimulated gastric acid secretion in the dog by activation of the autonomic (sympathetic) nervous system.

Intracerebroventricular administration of human calcitonin and human calcitonin gene-related peptide inhibits meal-stimulated gastric acid secretion in the dog.

H. Jurgen Lenz

Papers

Calcitonin gene-related peptide acts within the central nervous system to inhibit gastric acid secretion

Inhibition of gastric acid secretion by brain peptides in the dog. Role of the autonomic nervous system and gastrin.

Intracerebroventricular administration of human calcitonin and human calcitonin gene-related peptide inhibits meal-stimulated gastric acid secretion in the dog.