Journal
ELIFE
Volume 10, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.66170
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Funding
- NIDCR NIH HHS [R01 DE014756, R56 DE014756, R01 DE019245, F31 DE030670] Funding Source: Medline
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In this study, researchers found that the Ca2+ signals in salivary secretion process in live mice initiate in the apical endoplasmic reticulum, forming highly localized trains of transient that fail to fully propagate, leading to large apical-basal gradients following optimal stimuli for secretion. A new mathematical model incorporating these findings will help to understand how salivary secretion can be optimally stimulated by apical Ca2+ signals.
Salivary fluid secretion involves an intricate choreography of membrane transporters to result in the trans-epithelial movement of NaCl and water into the acinus lumen. Current models are largely based on experimental observations in enzymatically isolated cells where the Ca2+ signal invariably propagates globally and thus appears ideally suited to activate spatially separated Cl and K channels, present on the apical and basolateral plasma membrane, respectively. We monitored Ca2+ signals and salivary secretion in live mice expressing GCamp6F, following stimulation of the nerves innervating the submandibular gland. Consistent with in vitro studies, Ca2+ signals were initiated in the apical endoplasmic reticulum. In marked contrast to in vitro data, highly localized trains of Ca2+ transients that failed to fully propagate from the apical region were observed. Following stimuli optimum for secretion, large apical-basal gradients were elicited. A new mathematical model, incorporating these data was constructed to probe how salivary secretion can be optimally stimulated by apical Ca2+ signals.
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