Related Experiment Video

Updated: Jul 14, 2026

Live-cell Measurement of Odorant Receptor Activation Using a Real-time cAMP Assay
09:11

Live-cell Measurement of Odorant Receptor Activation Using a Real-time cAMP Assay

Published on: October 2, 2017

The STC-1 cells express functional orexin-A receptors coupled to CCK release

K P Larsson1, K E Akerman, J Magga

  • 1The Cell Biology, Research Group, Department of Neurobiology, University of Kuopio, FIN-70211 Kuopio, Finland.

Biochemical and Biophysical Research Communications
|August 29, 2003
PubMed

Insights

Orexin-A stimulates cholecystokinin (CCK) release from gut neuroendocrine cells. This process involves cell membrane depolarization and calcium channel activation, revealing a novel neuroendocrine function for orexins.

Area of Science:

  • Neuroendocrinology
  • Gastrointestinal Physiology

Background:

  • Orexins are neuropeptides involved in feeding and vigilance.
  • Orexins are found in gut neuroendocrine cells, but their function there is unclear.
  • The STC-1 cell line serves as a model for intestinal neuroendocrine cells.

Purpose of the Study:

  • To investigate the effects of orexin-A on the STC-1 cell line.
  • To elucidate the signaling pathways involved in orexin-A's action on these cells.

Main Methods:

  • Reverse transcription polymerase chain reaction (RT-PCR) to detect orexin receptors.
  • Stimulation of STC-1 cells with orexin-A.
  • Measurement of cholecystokinin (CCK) release.
  • Assessment of intracellular calcium levels.
  • Electrophysiological recordings for membrane potential.
  • Analysis of cAMP and phosphoinositide turnover.

Main Results:

  • STC-1 cells express both OX(1) and OX(2) receptors.
  • Orexin-A induced a dose-dependent release of CCK.
  • CCK release was dependent on extracellular calcium and L-type calcium channels.
  • Orexin-A increased intracellular calcium and caused membrane depolarization.
  • Orexin-A did not affect cAMP or phosphoinositide levels.

Conclusions:

  • Orexin-A activates functional orexin receptors in STC-1 cells.
  • Orexin-A stimulates CCK release via membrane depolarization and L-type calcium channel activation.
  • This study reveals a novel neuroendocrine role for orexin-A in the gut.

More Related Videos

Identification of Orexin and Endocannabinoid Receptors in Adult Zebrafish Using Immunoperoxidase and Immunofluorescence Methods08:37

Identification of Orexin and Endocannabinoid Receptors in Adult Zebrafish Using Immunoperoxidase and Immunofluorescence Methods

Published on: June 25, 2019

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels07:17

Single-Cell Calcium Imaging for Studying the Activation of Calcium Ion Channels

Published on: December 13, 2024

Related Concept Videos

G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...
Sleep-Wake Cycles01:24

Sleep-Wake Cycles

Sleep is an essential physiological process vital to maintaining overall well-being. The reticular activating system (RAS), a network of neurons in the brainstem, regulates wakefulness and sleep. While it may seem passive, sleep consists of distinct cycles, each with its unique characteristics and functions. Two key sleep phases are non-rapid eye movement (NREM) and  rapid eye movement (REM).
NREM Sleep
NREM sleep comprises four progressive stages that seamlessly merge:
Opioid Receptors: Overview01:22

Opioid Receptors: Overview

Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2, D-Pen5]-enkephalin or DPDPE for...
Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...