Fig. 5.
Tranexamic acid (TXA) had no impact on the amplitude of basal synaptic transmission but prolonged current decay and thereby increased charge transfer. Principal neurons of the basolateral amygdala were held at a holding potential of −70 mV. Compound postsynaptic currents evoked by electrical stimulation (cePSCs) of the external capsule were recorded. (A) Peak amplitudes of cePSCs remained unaffected by TXA (92 ± 7% of control; n = 6; t test: P = 0.481). Inset shows representative recording traces. (B) Current decay was fitted exponentially and was prolonged from 18.4 ± 2.8 ms under control conditions to 23.6 ± 3.6 ms in the presence of 1 mM TXA (n = 6; t test: P = 0.032). (C) Charge transfer (area under the curve of the recording trace) was increased to 119 ± 5% (n = 6; signed rank test: P = 0.023). *P < 0.05.