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The Role of Gap Junctions in Lacrimal Acinar Cells: The Formation of Tears

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Lacrimal Gland, Tear Film, and Dry Eye Syndromes 3

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 506))

Abstract

Water movement in the lacrimal gland is a consequence of ion channel and transporter activity. The production of tears is a consequence of acetylcholine (Ach) stimulation of acinar and duct cells, which produce a transepithelial flux of ions resulting in fluid movement. Ach acts through phospholipase C via Gq/11 and subsequently results in elevation of intracellular IP3 and DAG. The former raises intracellular calcium while the latter activates many PKC isoforms (Walcott, 1998; Dartt et al., 1998). In lacrimal gland K+, chloride and cation channels are activated by elevated intracellular calcium (Marty et al., 1984; Begenisich and Melvin, 1998).

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References

  • Azzarolo, A.M., R.L. Wood et al. Androgen influence on lacrimal gland apoptosis, necrosis, and lymphocytic infiltrations. Invest Ophthalmol Vis Sci. 40:592–602 1999.

    CAS  PubMed  Google Scholar 

  • Begenisich, T., and J.E. Melvin. Regulation of chloride channels in secretory epithelium. J Mem Biol. 163:77–86 1998.

    Article  CAS  Google Scholar 

  • Brink, P.R., K. Cronin, K. Banach, E. Peterson, E.M. Westphale, K.H. Seul, S.V. Ramanan, and E.C. Beyer. Evidence for heteromeric gap junction channels composed of hCx37 and rCx43. Amer J Physiol. 273:C1386–C1396 1997.

    Google Scholar 

  • Dartt, D.A., R.R. Hodges, and D. Zoukhri. Signal transduction pathways activated by cholinergic and alpha adrenergic agonists in the lacrimal gland. Ad Exp Med and Biol. 438:113–121 1998.

    Article  CAS  Google Scholar 

  • Delage, B and J. Deleze. A reexamination of calcium effects on gap junctions in heart myoctyes. In: Gap Junctions Edited by C. Perrachia. Current Topics in Membranes 49:189–206 2000.

    Google Scholar 

  • Kwak, B.R., T.A. Vanveen, L.J. Analbars, and H.J. Jongsma. TPA increases conductance but decreases permeability in neonatal rat cardiomyocyte gap junction channels. Exp Cell Res. 220:456–463 1995.

    Article  CAS  PubMed  Google Scholar 

  • Marty, A., Y.P. Tan, and A. Trautmann. Three types of calcium-dependent channel in rat lacrimal gland. J Physiol. 357:293–326 1984.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Moore et al., in press.

    Google Scholar 

  • Neyton, J and A. Trautmann. Acetylcholine modulation of the conductance of intercellular junctions between rat lacrimal cells. J Physiol. 377:283–293 1986.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Randriamampita, C, C Giaume, J. Neyton, and A. Trautmann. Acetycholine-induced closure of gap junction channels in rat lacrimal gland is probably mediated by PKC. Pfluger Archiv. 412:462–468 1988.

    Article  CAS  Google Scholar 

  • Sullivan, D.A., M.R. Allansmith et al. Hormonal influence on the secretory immune system of the eye: androgen modulation of IgA levels in tears of rats. J Immunol. 134:2978–2982 1985.

    CAS  PubMed  Google Scholar 

  • Sullivan, D., K.L. Krenzer et al. Does androgen insufficiency cause lacrimal gland inflammation and aqueous tear deficiency? Invest Ophthalmol Vis Sci. 40:1261–1265 1999.

    CAS  PubMed  Google Scholar 

  • Valiunas, V., H. Niessen, K. Willecke, and R. Weingart. Electrophysiological properties of gap junction channels in hepatocytes isolated from Cx32-deficient and wild-type mice. Pflugers Arch. 437:846–856 1999.

    Article  CAS  PubMed  Google Scholar 

  • Walcott, B. The lacrimal gland and its veil of tears. New Physiol Sci. 13:97–103 1998.

    CAS  Google Scholar 

  • Walcott, B., N. Claros, A. Patel, and P.R. Brink. Carbachol induced protein secretion from normal and Sjøgren’s mouse model lacrimal glands. Assoc Res Vis and Ophthalmol. 1997.

    Google Scholar 

  • Warren, D.W., A.M. Azzarolo et al. Androgen support of lacrimal gland function in the female rabbit. Ad Exp Med Biol. 438:89–94 1998.

    Article  CAS  Google Scholar 

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© 2002 Kluwer Academic/Plenum Publishers

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Brink, P.R., Valiunas, V., Moore, L., Birzgalis, A., Walcott, B. (2002). The Role of Gap Junctions in Lacrimal Acinar Cells: The Formation of Tears. In: Sullivan, D.A., Stern, M.E., Tsubota, K., Dartt, D.A., Sullivan, R.M., Bromberg, B.B. (eds) Lacrimal Gland, Tear Film, and Dry Eye Syndromes 3. Advances in Experimental Medicine and Biology, vol 506. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0717-8_14

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  • DOI: https://doi.org/10.1007/978-1-4615-0717-8_14

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5208-2

  • Online ISBN: 978-1-4615-0717-8

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