December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Sodium Potassium Di-chloride Co-transporter (NKCC1) In Mouse Lacrimal Gland
Author Affiliations & Notes
  • B Walcott
    Neurobiology & Behavior SUNY at Stony Brook Stony Brook NY
  • C Picken
    Physiology and Biophysics SUNY Stony Brook Stony Brook NY
  • LC Moore
    Physiology and Biophysics SUNY Stony Brook Stony Brook NY
  • PR Brink
    Physiology and Biophysics SUNY Stony Brook Stony Brook NY
  • Footnotes
    Commercial Relationships   B. Walcott, None; C. Picken, None; L.C. Moore, None; P.R. Brink, None. Grant Identification: EY09406
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3116. doi:
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    • Get Citation

      B Walcott, C Picken, LC Moore, PR Brink; Sodium Potassium Di-chloride Co-transporter (NKCC1) In Mouse Lacrimal Gland . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3116.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose:To determine if the sodium potassium di-chloride co-transporter is expressed in mouse lacrimal gland and if it has a role in fluid secretion. Methods:Immunocytochemistry was used to localize the co-transporter in frozen sections of exorbital lacrimal glands. Furosemide, a specific blocker of the co-transporter, was used on isolated cells and intact glands to determine the effects on fluid secretion. Results:Immunocytochemistry using either of two antibodies to the NKCC1 co-transporter, one courtesy of R.J. Turner and the other of E. Delpire, showed significant staining of the mouse lacrimal gland. Duct cells showed intense staining of the basolateral membranes while acinar cell membranes had definite but less intense staining. Isolated cells, when exposed to a 1 microM carbachol isotonic saline solution, will rapidly shrink by about 10% due to an efflux of ions and water. Furosemide (50 microM), a blocker of the NKCC1 co-transporter, applied in isotonic saline also caused the cells to shrink but at a much slower rate than carbachol. Isolated cells exposed to hypertonic saline showed a regulatory volume increase (RVI). Furosemide significantly reduced RVI. Furosemide applied to glands in situ reduced the carbachol induced fluid flow by about 50%. Conclusion:The sodium potassium di-chloride co-transporter (NKCC1) is present in mouse exorbital lacrimal gland acinar and duct cells. Blocking the NKCC1 caused isolated cells to shrink.This suggests that there may be a basal leakage of chloride ions from these cells and that the chloride is replaced by the co-tranporter. Such a basal leakage if it occurred in the intact gland could cause a basal fluid secretion in the absence of neural stimulation. The effect of blocking NKCC1 on the RVI and on fluid secretion from the intact glands shows that the activity of NKCC1 is necessary for the normal fluid secretion by the lacrimal gland

Keywords: 452 lacrimal gland • 446 ion transporters 

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