Fig. 6.
α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) receptor–mediated currents remained unaffected by tranexamic acid (TXA). (A) AMPA receptor–mediated excitatory postsynaptic currents (AMPA-EPSCs) were recorded in the presence of 3-amino-propyl(diethoxymethyl)phosphinic acid (CGP35348; 200 μM), bicuculline methiodide (20 μM), and d(−)-2-amino-5-phosphonopentanoic acid (AP5; 50 μM). The peak amplitudes of AMPA-EPSCs did not change (97 ± 5% of control; n = 5; t test: P = 0.511) when TXA (1 mM) was bath-applied. (Ai) Shows representative recording traces. (Aii) TXA did not affect AMPA-EPSCs when it was applied at a concentration of 5 mM. (B) NMDA-EPSCs were recorded at a holding potential of −40 mV in the presence of CGP35348 (200 μM), bicuculline methiodide (20 μM), and 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulphonamide (NBQX; 5 μM). The application of 1 mM TXA did not result in changed peak amplitudes of NMDA-EPSCs (103 ± 9% of control; n = 5; t test: P = 0.706). (Bi) Shows representative recording traces. (Bii) TXA did not affect NMDA-EPSCs when it was applied at a concentration of 5 mM.