Capacitative calcium entry in parotid acinar cells

Area of Science:

• Cellular Physiology
• Calcium Signaling
• Membrane Transport

Background:

• Parotid acinar cells play a crucial role in secretion.
• Intracellular calcium ([Ca2+]) dynamics are central to cell signaling.
• Understanding calcium influx mechanisms is vital for cellular function.

Purpose of the Study:

• To investigate the effect of intracellular calcium pool depletion on calcium influx in parotid acinar cells.
• To determine the relationship between agonist stimulation and subsequent calcium entry.
• To elucidate the mechanism underlying receptor-activated calcium entry.

Main Methods:

• Utilized the intracellular Ca2+ indicator fura-2 to monitor cytosolic [Ca2+].
• Manipulated extracellular and intracellular Ca2+ concentrations.
• Employed muscarinic agonists and the antagonist atropine to control cellular stimulation and calcium pool status.

Main Results:

• Prior activation and subsequent depletion of the agonist-sensitive intracellular Ca2+ pool led to a faster and larger increase in cytosolic [Ca2+] upon Ca2+ restoration.
• This enhanced Ca2+ influx persisted even after prolonged intervals.
• Refilling the depleted pool abolished the rapid Ca2+ influx, resembling unstimulated cells.

Conclusions:

• Agonist-induced emptying of the intracellular Ca2+ pool significantly increases plasma membrane permeability to Ca2+.
• This enhanced Ca2+ influx appears to be a direct consequence of the depleted pool state, independent of second messengers like inositol phosphates.
• The study suggests that the emptying of agonist-sensitive Ca2+ pools is a key factor in receptor-activated Ca2+ entry.