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International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN Print: 2155-014X
ISSN Online: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v8.i4.10
pages 291-297

Subunit-Specific Modulation of α1 Glycine Receptors by Ginkgolic Acid

Galina Maleeva
Aix Marseille University, INSERM UMR1106, INS, Inst Neurosci Syst, Marseille, France; Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Svetlana Buldakova
Aix Marseille University, INSERM UMR1106, INS, Inst Neurosci Syst, Marseille, France
Piotr Bregestovski
Aix Marseille University, INSERM UMR1106, INS, Inst Neurosci Syst, Marseille, France

ABSTRACT

Ginkgo biloba extract is a multicomponent pharmacological agent widely used in neurological disorders therapy. Ginkgolic acid, a constituent of lipophylic Ginkgo biloba extract, is known to have numerous biological activities. In the present study, using whole-cell configuration of patch-clamp recording, we have analyzed the effect of ginkgolic acid on glycine receptors, postsynaptic ion channel proteins that provide the fast inhibitory neurotransmission in nervous system of vertebrates. The experiments were performed on cultured chinese hamster ovary cells (CHO cells), transfected with α1 or α2 subunits of glycine receptor. Ionic currents were induced by the fast application of different glycine concentrations. After 20 − 40 sec of pre-treatment with ginkgolic acid (25μM), currents mediated by α1 glycine receptors reversibly increased from (364 ± 49) pA, (n = 34) to (846 ± 134) pA, (n = 34). EC50 for glycine has changed from (36 ± 6) μM, in control, to (17 ± 2) μM under ginkgolic acid action. In contrast, the application of ginkgolic acid on glycine receptors formed by α2 subunits did not provoke potentiation. Our results demonstrate that ginkgolic acid is a subunit-specific modulator of glycine receptors. The mechanisms of the ginkgolic acid action on glycine receptors require further investigation.


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