ムスカリン受容体を介する細胞内シグナルと唾液分泌能の回復・維持・促進

抄録

Oral sensory stimuli including taste and mastication have been shown to elicit salivation via the autonomic nervous system. Studies using salivary acinar cells have revealed the roles of muscarinic receptor-mediated Ca²⁺ response in the secretion driven by Cl^- transports. It is also known that activation of the cAMP system via the β-adrenergic stimulation leads to the exocytotic protein secretions. In addition, the autonomic nervous system is likely to contribute to maintain functions of salivary glands. Examples are known as; the atrophy of the salivary glands due to a liquid diet and its recovery with a solid diet; compensatory hypertrophy of the contralateral side due to dysfunction of the salivary gland on one side.

We are trying to elucidate the mechanisms of salivary secretion and the maintenance and recovery of salivary gland functions using in vivo experimental systems that allow to analyze Ca²⁺ response and blood flow in the submandibular gland of live rats. In addition, possible involvement of the muscarinic receptor-mediated ERK phosphorylation in salivary gland functions are examined. The possibility and importance of a new therapies aimed at "recovery and enhancement" of physiological salivary secretion by controlling the mechanisms that maintain salivary secretory activity will be discussed.