Ca2+ mobilization by nicotine through synaptic activation in rat parotid acini

Nicotine has been reported to increase the intracellular Ca2+ concentration ([Ca2+]i) in sublingual acini due to neurotransmitter release from nerve terminals associated with the cell preparation (1). However, it is unclear whether or not the same reaction exists in parotid cells. Therefore, we investigated effect of nicotine on Ca2+ mobilization in digested parotid acini from rats. After removing the parotid gland from Wistar rats, the tissues were minced and digested with collagenase. Then, the intracellular Ca2+ indicator fura-2 was added to the preparation, and the change in [Ca2+]i was monitored using fluorescent microscope. In many but not all parotid acini, K+ stimulation induced transient increases in [Ca2+]i. The K+-induced Ca2+ response in parotid acini was completely blocked by Cd2+-containing solution. These results suggest that the parotid cell preparation has nerve terminals. In all high-K+-sensitive parotid acini, over 3μM of nicotine increased [Ca2+]i, and the response was blocked by a Cd2+-containing solution and nicotinic receptor antagonists. All high-K+-insensitive acinar cells were resistant to the effect of nicotine on Ca2+ mobilization. These results suggest that nicotine induces increases in [Ca2+]i in parotid acini due to neurotransmitter release from associated nerve terminals.