PMID: 11316256Apr 24, 2001Paper

Forskolin modulation of desensitization at GABA(A) and glycine receptors is not mediated by cAMP-dependent protein kinase in isolated carp amacrine-like cells

Pflügers Archiv : European journal of physiology
P Li, X L Yang

Abstract

The effects of forskolin on gamma-aminobutyric acid type-A (GABA(A)) and glycine receptors in amacrine-like cells of carp (Carassius auratus) retina were studied using patch-clamp techniques. Application of 50 microM forskolin markedly accelerated the desensitization of whole-cell responses induced by 100 microM GABA or glycine without changing the peak amplitude of the response. Both 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) and 3-isobutyl-1 -methylxanthine (IBMX) (500 microM) failed to accelerate the desensitization of these two receptors. Protein kinase A (PKA) inhibitors, N- [2-[(p-bromocinnamyl)amino]ethyl)-5-isoquinolinesulfonamide dihydrochloride (H-89) and N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-8), could not block these effects of forskolin. An inactive analogue of forskolin, 1,9-dideoxyforskolin (DFSK), accelerated the desensitization effectively. These results suggest that forskolin's effects are not mediated by activation of the PKA pathway. Moreover, similar results were obtained using excised outside-out patches of these cells, suggesting that forskolin may act on an extracellular site(s). The neurosteroids 5alpha-pregnane-3alpha,21 -diol-20-one (THDOC) and 5-pregnen-31 ...Continue Reading

Citations

Feb 27, 2003·The European Journal of Neuroscience·Dominique Chesnoy-Marchais
Jun 6, 2018·Frontiers in Molecular Neuroscience·Ulrike BreitingerHans-Georg Breitinger
Jul 31, 2002·Archives of Biochemistry and Biophysics·Murat OzCharles E Spivak

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