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Pancreatic acinar cells: the acetylcholine equilibrium potential and its ionic dependency
The Journal of Physiology
|August 1, 1977
Summary
Acetylcholine (ACh) stimulation in pancreatic acinar cells increases permeability to sodium, potassium, and chloride ions. This ion flux, particularly sodium and chloride influx, underlies ACh-evoked potential changes in these cells.
Area of Science:
- Cellular Electrophysiology
- Pancreatic Physiology
- Neurotransmitter Signaling
Background:
- Pancreatic acinar cells respond to acetylcholine (ACh), a key neurotransmitter.
- Understanding the ionic mechanisms of ACh signaling is crucial for pancreatic function.
Purpose of the Study:
- To investigate the electrophysiological effects of ACh on pancreatic acinar cells.
- To determine the ion permeability changes induced by ACh stimulation.
Main Methods:
- In vitro electrophysiological recordings using micro-electrodes in rat and mouse pancreatic acinar cells.
- Measurement of membrane potential, resistance, and current-voltage relationships.
- Application of varying membrane potentials and ion composition changes in superfusion fluid.
Main Results:
- ACh stimulation evoked dose-dependent changes in membrane potential, with the reversal potential (E(ACh)) varying with extracellular ion concentrations.
- Replacing extracellular chloride with sulfate shifted E(ACh) positively, indicating chloride's role.
- Goldman analysis suggested ACh increases membrane permeability to Na+, K+, and Cl-, with relative permeabilities P(Na)/P(K) = 2.5 and P(Cl)/P(K) = 5.
Conclusions:
- ACh increases pancreatic acinar cell membrane permeability to Na+, K+, and Cl-.
- The primary ionic events are Na+ and Cl- influx, with a smaller K+ efflux.
- These ion movements mediate the electrophysiological response to ACh in pancreatic acinar cells.