Ca²⁺ signalling in the endoplasmic reticulum/secretory granule microdomain

Area of Science:

• Cell Biology
• Physiology
• Neuroscience

Background:

• Calcium (Ca2+) microdomains were first identified in nerve terminals in 1992.
• Their presence in pancreatic acinar cells was established in 1993.
• Pancreatic acinar cells utilize Ca2+ signaling for precise control of digestive enzyme secretion.

Purpose of the Study:

• To review the characteristics of apical Ca2+ signaling microdomains in pancreatic acinar cells.
• To emphasize the passive and active Ca2+ buffering properties within these microdomains.
• To discuss the role of Ca2+-induced Ca2+ release in apical signaling.

Main Methods:

• Review of existing literature on Ca2+ microdomains and pancreatic acinar cell function.
• Discussion of Ca2+ signaling mechanisms, including release from endoplasmic reticulum (ER) terminals.
• Analysis of Ca2+ buffering and Ca2+-induced Ca2+ release within the apical domain.

Main Results:

• Apical microdomains in pancreatic acinar cells are dominated by secretory granules.
• Local Ca2+ signaling involves repetitive Ca2+ release from apical ER terminals, sustained by diffusion from the basolateral ER store.
• These microdomains exhibit specific buffering properties and respond to local Ca2+ elevations via Ca2+-induced Ca2+ release.

Conclusions:

• The unique characteristics of apical Ca2+ signaling microdomains are crucial for appropriate Ca2+ spiking in pancreatic acinar cells.
• Disruption of these microdomains can lead to pathophysiological consequences.
• Understanding these microdomains is vital for comprehending pancreatic exocrine function and disease.