December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Calcium Signalling Domains in the Intact Human Lens
Author Affiliations & Notes
  • G Duncan
    School of Biological Sciences University of East Anglia Norwich United Kingdom
  • DJ Collison
    School of Biological Sciences University of East Anglia Norwich United Kingdom
  • Footnotes
    Commercial Relationships   G. Duncan, None; D.J. Collison, None. Grant Identification: Medical Research Council, UK
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2989. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      G Duncan, DJ Collison; Calcium Signalling Domains in the Intact Human Lens . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2989.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: Calcium signalling receptor systems are not uniformly distributed in the intact human lens (Collison & Duncan, IOVS. 2001;42:2356-2363). This study therefore investigated the regional distribution of membrane-associated, signal-amplifying calcium entry pathways. Methods: The lens was dissected from donor eyes (20-80 yrs), placed anterior face down in a plastic chamber and perifused with artificial aqueous humour at 30C. Following Fura-2 incorporation into anterior and equatorial epithelial cells, cytosolic calcium levels were monitored using epifluorescence techniques. Calcium entry was monitored in the resting lens, and following activation of G-protein and tyrosine-kinase signalling systems. The blocking effects of LaCl on store-mediated calcium entry, flufenamic acid on non-selective cation entry, and nifedipine on voltage-gated calcium channels were also investigated. Results: In the anterior region, sustained G-protein receptor activation (e.g. histamine, 10-100 µM) led to a maintained increase in cytosolic calcium that was inhibited by addition of LaCl (10 µM), but insensitive to nifedipine (10 µM). In the equatorial region, both G-protein (histamine, 10-100 µM) and tyrosine-kinase (EGF, 10 ng/ml) receptor activation gave rise to maintained calcium increases that were abolished by LaCl, but not by nifedipine. In this region the resting calcium level was significantly reduced in the presence of flufenamic acid (50 µM), indicating the presence of a calcium entry pathway in unstimulated cells. LaCl or nifedipine had no effect on the resting calcium levels in either anterior or equatorial epithelial cells. Furthermore, exposure to flufenamic acid had only a minor effect on resting levels in anterior cells. Conclusion: The stimulated store-mediated calcium entry pathway amplifies receptor-mediated calcium signals in both anterior and equatorial cells. However, a novel, resting, flufenamic acid-sensitive pathway plays a major role only in the equatorial region and will contribute to ion current asymmetries in the intact lens.

Keywords: 581 signal transduction: pharmacology/physiology • 334 calcium • 445 ion channels 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×