Abstract
Lacrimal gland protein secretion is primarily under the control of cholinergic muscarinic and αl-adrenergic receptors.1 Cholinergic agonists are coupled to the activation of phospholipase C (PLC),2 which leads to the production of two second messenger molecules: inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 increases the cytoplasmic concentration of calcium ([Ca2+]i) and DAG activates protein kinase C (PKC), two events that are thought to trigger protein secretion.1 Lacrimal gland αl-adrenergic receptors are of particular interest. Unlike those in other tissues, they are not coupled to the PLC pathway, although their activation leads to a slight increase in [Ca2+]i.3 We have also shown that these receptors are not linked to the activation of phospholipase D in lacrimal gland acini.4 Thus the transduction pathway(s) used by the α1-adrenergic receptors to trigger lacrimal gland protein secretion remains to be identified.
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References
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Zoukhri, D., Hodges, R.R., Sergheraert, C., Dartt, D.A. (1998). Protein Kinase C Isoforms Differentially Control Lacrimal Gland Functions. In: Sullivan, D.A., Dartt, D.A., Meneray, M.A. (eds) Lacrimal Gland, Tear Film, and Dry Eye Syndromes 2. Advances in Experimental Medicine and Biology, vol 438. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5359-5_26
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DOI: https://doi.org/10.1007/978-1-4615-5359-5_26
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