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Acetylcholine-induced, calcium-dependent norepinephrine outflow from peripheral human lymphocytes
N R Musso1, S Brenci, F Indiveri
1Department of Internal Medicine, San Martino Hospital, Genoa, Italy. nrmusso@unige.it
Journal of Neuroimmunology
|July 22, 1998
Summary
Peripheral human lymphocytes release norepinephrine (NE) in response to acetylcholine (ACh) and calcium influx. This study investigated the mechanisms of NE outflow, revealing a calcium-dependent process mediated by nicotinic receptors.
Area of Science:
- Neuroimmunology
- Cellular Signaling
- Pharmacology
Background:
- Catecholamines (CA) play crucial roles in cellular communication.
- Understanding catecholamine release from human lymphocytes is vital for neuroimmunology.
- Previous research has not fully elucidated the mechanisms of norepinephrine (NE) outflow from lymphocytes.
Purpose of the Study:
- To investigate the release of catecholamines, specifically norepinephrine (NE), from peripheral human lymphocytes.
- To determine the effects of L-tyrosine and L-Dopa on intracellular NE levels.
- To examine the influence of acetylcholine (ACh), Veratridine, Ionomycin, and KCl on NE outflow, and the role of calcium and cholinergic receptors in this process.
Main Methods:
- Peripheral human lymphocytes were incubated with L-tyrosine and L-Dopa.
- The release of NE into the supernatant was measured after stimulation with ACh, Veratridine, Ionomycin, or KCl.
- High-performance liquid chromatography with electrochemical detection (HPLC-ECD) was used to quantify NE.
- The effects of methoxyverapamil (D600, a Ca2+ channel blocker) and cholinergic antagonists (Tetraethylammonium and atropine) on ACh-induced NE outflow were assessed.
Main Results:
- L-Tyrosine and L-Dopa significantly increased intracellular NE but did not induce NE outflow.
- ACh, Veratridine, Ionomycin, and KCl stimulated a detectable outflow of NE from lymphocytes.
- Methoxyverapamil (D600) significantly reduced ACh-induced NE outflow, indicating a role for calcium channels.
- Tetraethylammonium (a nicotinic antagonist) significantly decreased ACh-induced NE outflow, while atropine (a muscarinic antagonist) did not.
Conclusions:
- Norepinephrine (NE) outflow from peripheral human lymphocytes is a demonstrable phenomenon.
- NE secretion is dependent on acetylcholine (ACh) acting via nicotinic receptors and calcium influx.
- Stimulators like Veratridine, Ionomycin, and KCl facilitate NE release by promoting calcium entry into lymphocytes.