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Published on: September 20, 2011
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
Summary
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.
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.
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