Fig. 1
From: Frequency-dependent gating of feedforward inhibition in thalamofrontal synapses
The thalamofrontal integration window increases at high frequency. a Representative traces of the synaptic current. An inhibitory postsynaptic current (IPSC) measured at 0 mV (outward black trace) and an IPSC in the presence of a GABAA receptor antagonist (2 μM bicuculline, green trace). An EPSC measured at − 70 mV (inward black trace) and an EPSC in the presence of 10 μM 6-cyano-7-nitroquinoxaline (CNQX; orange trace). An NMDA channel-dependent current was ruled out by 100 μM (2R)-amino-5-phosphonopentanoate (APV) throughout the experiment. Magnified EPSC and IPSC traces around the onset of the synaptic currents (inset). The inflection points of the EPSC and IPSC were defined as the onsets and used to calculate the onset latencies. b The onset latency of the thalamofrontal IPSC on pyramidal cells was longer than that of the EPSC (17 cells, ***p = 0.0008, paired t-test, parametric). c Example trace of the EPSC/IPSC complex sequence at − 30 mV with 5 Hz optogenetic thalamofrontal stimulation. d An example trace showing how the integration window was measured, namely, as the duration of the net inward current in EPSC-IPSC sequences. e An EPSC-IPSC sequence with and without 2 μM bicuculline (Vhold = − 30 mV, red). f−g The normalized length of the integration window at 5 Hz (f) (9 cells, *Pstim2 = 0.023, **Pstim3 = 0.0039, *Pstim4 = 0.012, **Pstim5 = 0.0078, paired t-test, non-parametric) and 10 Hz (g) (9 cells, *Pstim2 = 0.016, **Pstim3 = 0.0078, **Pstim4 = 0.0039, **Pstim5 = 0.0078, paired t-test, non-parametric)