These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Pancreatic acinar cells: electrophysiological evidence for stimulant-evoked increase in membrane calcium permeability in the mouse.
    Author: Laugier R, Petersen OH.
    Journal: J Physiol; 1980 Jun; 303():61-72. PubMed ID: 7431246.
    Abstract:
    1. Membrane potential and resistance were measured in acini from superfused isolated segments of mouse pancreas using two micro-electrodes inserted into neighbouring acinar cells. Stimulation was carried out exposing segments to 5 x 10(-7) M-acetylcholine (ACh) or 3 x 10(-7) M-pentagastrin. 2. Sustained stimulation with ACh or pentagastrin caused sustained membrane depolarization and resistance reduction. For periods of stimulation up to 15 min there was no sign of desensitization. 3. Sustaind stimulation during exposure of the tissue to a Ca-free solution containing EGTA (ethylene glycol bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid) resulted only in a transient depolarization and resistance reduction. 4. Removal of external Ca during sustained stimulation resulted in immediate hyperpolarization and increase in resistance. Readmission of Ca, still during exposure to ACh or pentagastrin, depolarized the membrane and reduced the resistance. Mn could not mimic this effect of Ca. 5. Removal of external Ca in the absence of stimulation evoked depolarization and membrane resistance reduction. 6. It is concluded that sustained stimulation of pancreatic acinar cells with cholinergic agents or peptides of the cholecystokinin-gastrin group evokes an increase in the Ca permeability of the plasma membrane. Ca entering the cells from the outside is important in maintaining ion channels in their open state, thus sustaining the stimulant-evoked depolarization and resistance reduction. The initial stimulant-evoked membrane response, however, seems to be triggered by release of Ca from internal stores and is independent of external Ca.
    [Abstract] [Full Text] [Related] [New Search]