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Research ArticleNEUROPHARMACOLOGY

Tranexamic Acid, a Widely Used Antifibrinolytic Agent, Causes Convulsions by a γ-Aminobutyric AcidA Receptor Antagonistic Effect

Roman Furtmüller, Michael G. Schlag, Michael Berger, Rudolf Hopf, Sigismund Huck, Werner Sieghart and Heinz Redl
Journal of Pharmacology and Experimental Therapeutics April 2002, 301 (1) 168-173; DOI: https://doi.org/10.1124/jpet.301.1.168
Roman Furtmüller
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Michael G. Schlag
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Michael Berger
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Rudolf Hopf
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Sigismund Huck
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Werner Sieghart
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Heinz Redl
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Abstract

Application of 4-(aminomethyl)cyclohexanecarboxylic acid (tranexamic acid; TAMCA) to the central nervous system (CNS) has been shown to result in hyperexcitability and convulsions. However, the mechanisms underlying this action are unknown. In the present study, we demonstrate that TAMCA binds to the γ-aminobutyric acid (GABA) binding site of GABAA receptors in membranes from rat cerebral cortex and does not interfere withN-methyl-d-aspartate receptors. Patch-clamp studies using human embryonic kidney cells transiently transfected with recombinant GABAA receptors composed of α1β2γ2 subunits showed that TAMCA did not activate these receptors but dose dependently blocked GABA-induced chloride ion flux with an IC50 of 7.1 ± 3.1 mM. Application of TAMCA to the lumbar spinal cord of rats resulted in dose-dependent hyperexcitability, which was completely blocked by coapplication of the GABAA receptor agonist muscimol. These results indicate that TAMCA may induce hyperexcitability by blocking GABA-driven inhibition of the CNS.

Footnotes

  • The first and second author contributed equally to this study.

  • Abbreviations:
    TAMCA (tranexamic acid)
    4-(aminomethyl)cyclohexanecarboxylic acid
    FS
    fibrin sealants
    CNS
    central nervous system
    NMDA
    N-methyl-d-aspartate
    GABAA
    γ-aminobutyric acidA
    [3H]MK-801
    (5S,10R)-(+)-5-methyl-[3,7-3H]-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine
    HEK
    human embryonic kidney
    TC50
    50 mM Tris-citrate buffer, pH 7.4
    HL
    hind limb
    PBS
    phosphate-buffered saline
    EGFP
    enhanced green fluorescent protein
    EMG
    electromyogram
    • Received August 21, 2001.
    • Accepted December 20, 2001.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 301 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 301, Issue 1
1 Apr 2002
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Research ArticleNEUROPHARMACOLOGY

Tranexamic Acid, a Widely Used Antifibrinolytic Agent, Causes Convulsions by a γ-Aminobutyric AcidA Receptor Antagonistic Effect

Roman Furtmüller, Michael G. Schlag, Michael Berger, Rudolf Hopf, Sigismund Huck, Werner Sieghart and Heinz Redl
Journal of Pharmacology and Experimental Therapeutics April 1, 2002, 301 (1) 168-173; DOI: https://doi.org/10.1124/jpet.301.1.168

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Research ArticleNEUROPHARMACOLOGY

Tranexamic Acid, a Widely Used Antifibrinolytic Agent, Causes Convulsions by a γ-Aminobutyric AcidA Receptor Antagonistic Effect

Roman Furtmüller, Michael G. Schlag, Michael Berger, Rudolf Hopf, Sigismund Huck, Werner Sieghart and Heinz Redl
Journal of Pharmacology and Experimental Therapeutics April 1, 2002, 301 (1) 168-173; DOI: https://doi.org/10.1124/jpet.301.1.168
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