Inhibitory synaptic transmission was dose-dependently reduced in the presence of tranexamic acid (TXA). γ-Aminobutyric acid receptor type A (GABA_A)–mediated inhibitory postsynaptic currents (GABA_A-IPSCs) were recorded in the presence of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulphonamide (NBQX; 5 μM), 3-amino-propyl(diethoxymethyl)phosphinic acid (CGP35348) (CGP; 200 μM), and d(−)-2-amino-5-phosphonopentanoic acid (AP5; 50 μM). The currents were evoked upon either electrical stimulation of the external capsule (GABA_A-IPSCs) or focal photolytic release of GABA_A-pCs. (A) The application of TXA (1 mM) led to a reduction of GABA_A-IPSCs to 36 ± 3% of control (n = 9; t test: P < 0.001). In the presence of TXA (1 mM), photolytically evoked GABA_A-pCs were reduced to 41 ± 5% of control (n = 9; t test: P < 0.001). There was no difference in the TXA-mediated degree of reduction between GABA_A-IPSCs and GABA_A-pCs. Insets show representative recording traces. (B) Two consecutive GABA_A-IPSCs were evoked with interstimulus intervals (ISIs) of 50 and 150 ms, respectively. The paired-pulse ratio was evaluated as the ratio of the amplitudes of the first and second GABA_A-IPSC. Application of 1 mM TXA did not affect the paired-pulse ratio of GABA_A-IPSCs. Inset shows representative recording trace. (C) TXA was applied at concentrations of 0.1, 0.3, 1, 5 or 10 mM to investigate the dose-dependency of the TXA-mediated inhibition of GABA_A receptor–mediated currents. GABA_A-IPSCs and GABA_A-pCs were reduced by TXA at half maximal inhibitory concentrations of 0.76 mM (Hill, −0.8) and 0.84 mM (Hill, −1.0), respectively. ns = not significant (P > 0.05), pCs = photolytically evoked currents.