Related Experiment Video

Updated: Oct 17, 2026

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

Capsaicin-sensitive sensory neurons in healing gastric lesions induced by HCl in rats

K Takeuchi1, T Ohuchi, S Okabe

  • 1Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.

Digestive Diseases and Sciences
|December 1, 1994
PubMed

More Related Videos

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats07:12

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

Published on: January 21, 2020

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx06:05

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx

Published on: May 2, 2025

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Gastric Phase of Digestion01:26

Gastric Phase of Digestion

The gastric phase of digestion begins as soon as food enters the stomach. The incoming food bolus triggers neural and hormonal mechanisms, which last approximately 3 to 4 hours. During this phase, the stomach undergoes significant changes to prepare the food for further digestion and absorption.
When food enters the stomach, it stretches the stomach walls and activates stretch receptors. This triggers local reflexes of the enteric nervous system, mediated through the myenteric plexus. These...
Intestinal Phase of Digestion01:29

Intestinal Phase of Digestion

The intestinal phase of digestion is the third and final stage of the digestive process, occurring after the cephalic and gastric phases. It begins when chyme, a partially digested mixture of food and digestive enzymes, enters the small intestine from the stomach. This phase is crucial for nutrient absorption and involves complex hormonal and enzymatic interactions.
The arrival of the chyme in the small intestine distends the duodenum, which triggers the enterogastric reflex. This distension...
Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...