Signaling Mechanisms That Regulate Saliva Formation

Abstract

The precipitating event in the formation of saliva is the binding of neurotransmitter molecules to cell surface receptor proteins. The principal neurotransmitters involved are acetylcholine and norepinephrine that bind, respectively, to muscarinic-cholinergic, and a-and ,-adrenergic receptors. The transduction of the extracellular signal requires an integral membrane protein capable of binding GTP, a G protein, that specifically interacts with the receptor. The components of G protein transduction systems are fairly well studied, but the pathways by which signals are routed are just being recognized. Delineation of such routing pathways is essential to understanding the regulation of saliva formation.

Defects in muscarinic receptor-coupled signal transduction in isolated parotid gland cells after in vivo irradiation: evidence for a non-DNA target of radiation

“…When stimulated, these receptors, which are of 93% of the M3 subtype (Dai et al, 1991), induce Gqprotein-coupled activation of phospholipase C (PLC), which hydrolyses phosphatidyl-inositol-4,5-bisphosphate (PIP 2 ). This leads to the formation of inositol-1,4,5-trisphosphate (IP 3 ), which mobilises Ca 2 þ from intracellular stores, and diacylglycerol (DAG), which activates protein kinase C (PKC) (Nishizuka, 1992;Baum et al, 1993, Sawali et al, 1993). An increase in intracellular free Ca 2 þ (Ca 2 þ i ) concentration is the predominant mechanism triggering the fluid secretion from acinar cells (Melvin, 1999), whereas PKC activates the secretion of low amounts of proteins in the saliva (Tojyo et al, 1992).…”

<b>P2Y purinoceptors mediate ATP-induced changes in intracellular calcium and amylase release in acinar cells of mouse parotid </b><b>glands </b>

“…On the other hand, low concentrations of ATP did not stimulate amylase release, supporting the view that an increase in [Ca 2+ ] i is not a sufficient stimulus in rat parotid gland acinar cells (59). Therefore, further studies are from intracellular Ca 2+ stores, and subsequent entry of Ca 2+ across the plasma membrane via a capacitative entry mechanism (5,30,58). The initial phase of [Ca 2+ ] i response to a muscarinic agonist appeared to be due to IP 3 -induced Ca 2+ release from intracellular Ca 2+ stores (62).…”

Sjögren's syndrome and the epithelial target: A comprehensive review

“…Exocytosis of proteins, glycoproteins and mucins occurs upon fusion of secretory granules with the plasma membrane. The sum of these processes constitutes what is referred to as "regulated secretion" that can be triggered both by external biochemical molecules (agonists) and/or mechanical signals [51,52]. Examples of the former group include alpha-and beta-adrenergic agonists, cholinergic agonists, peptidenergics and vasoactive intestinal peptide, among others [52].…”