Impaired neurotransmitter release from lacrimal and salivary gland nerves of a murine model of Sjogren's syndrome

PURPOSE. To determine whether lacrimal and salivary gland nerves of an anim al model of Sjogren's syndrome, the MRL/lpr mouse, are able to release acet ylcholine. The second purpose was to determine whether activation of the la crimal gland nerves of the MRL/lpr mouse leads to protein secretion METHODS. Total saliva was collected for 10 minutes from the oral cavity of male and female MRL/lpr and MRL/+ mice, after intraperitoneal stimulation w ith pilocarpine and isoproterenol. Lacrimal and salivary gland lobules prep ared from 18-week-old MRL/lpr and MRL/+ mice were incubated in the presence of depolarizing KCL (75 mM) solution. Acetylcholine release and peroxidase secretion (a protein secreted by the lacrimal gland) were measured using a spectrofluorometric assay. RESULTS. Female, but not male, MRL/lpr mouse salivary glands were hyper-res ponsive to in vivo injection of secretagogues. These mice produced signific antly higher amounts of saliva than did age-matched MRL/+ mice. Lacrimal an d salivary gland nerves from 18-week-old MRL/+ mice released acetylcholine in response to a depolarizing KCI solution. In contrast, nerves in glands f rom 18-week-old MRL/lpr mice did not increase acetylcholine release in resp onse to the depolarizing solution. Moreover, lacrimal glands from 18-week-o ld MRL/+ mice were able to secrete peroxidase in response to a depolarizing KCI solution, whereas those from 18-week-old MRL/lpr could not. This was n ot due to a defect in the secretory process, because addition of an exogeno us secretagogue elicited peroxidase secretion from 18-week-old MRL/lpr as w ell as MRL/+ mice lacrimal glands. CONCLUSIONS. The results show that activation of nerves of lacrimal and sal ivary glands infiltrated with lymphocytes does not increase the release of neurotransmitters, which results in impaired secretion from these glands.