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Cyclic AMP and anionic currents in porcine ciliary epithelium.

J C Fleischhauer1, J L Bény, J Flammer

  • 1Laboratory of Ocular Pharmacology and Physiology, University Eye Clinic Basel, Mittlere Strasse 91, PO Box, CH-4012 Basel, Switzerland.

Klinische Monatsblatter Fur Augenheilkunde
|June 22, 2001
PubMed
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Cyclic adenosine monophosphate (cAMP) activates transmembrane anionic currents in porcine ciliary epithelium, causing membrane potential depolarization. This effect is inhibited by diisothiocyanatostilbene-2,2

Area of Science:

  • Physiology
  • Molecular Biology
  • Ocular Science

Background:

  • Investigating the role of cyclic adenosine monophosphate (cAMP) in regulating ion transport within the ciliary epithelium.
  • Understanding the mechanisms of transmembrane current activation in ocular tissues.

Purpose of the Study:

  • To determine if cAMP activates transmembrane anionic currents in isolated porcine ciliary body.
  • To elucidate the involvement of anionic channels in cAMP-mediated signaling in the ciliary epithelium.

Main Methods:

  • Utilized intracellular microelectrodes to measure membrane potential changes in porcine ciliary body.
  • Administered forskolin and 8-bromo-adenosine 3',5'-cyclic monophosphothioate (8-br-cAMP) to stimulate cAMP.
  • Assessed the impact of diisothiocyanatostilbene-2,2' disulfonic acid (DIDS), an anionic channel inhibitor, on membrane potential.

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Main Results:

  • Both forskolin and 8-br-cAMP significantly depolarized the ciliary epithelium membrane potential.
  • Diisothiocyanatostilbene-2,2' disulfonic acid (DIDS) significantly inhibited the cAMP-induced depolarization.
  • Observed depolarization of 11.8 mV with forskolin and 9.3 mV with 8-br-cAMP, reduced to ~1 mV with DIDS.

Conclusions:

  • Cyclic adenosine monophosphate (cAMP) induces membrane potential depolarization in the porcine ciliary epithelium.
  • The findings suggest that cAMP-mediated depolarization involves the activation of anionic channels or transporters.
  • This study provides evidence for a cAMP-dependent pathway regulating ion flux in the ciliary body.