Figure 1.
Distinct EPSC amplitudes and short-term plasticity of CA1 PC – FSINs vs. PC – O-LM cell synapses
(A and B) Averaged postsynaptic responses evoked by three action potentials (at 40 Hz) in presynaptic PCs are shown in O-LM cells (A, thin traces: 17 individual pairs; thick trace: the average of 96 pairs) and FSINs (B, thin traces: 16 individual pairs, thick trace: the average of 70 pairs). The amplitude of the first uEPSCs and the short-term plasticity of the responses show large variability within groups but are considerably different between O-LM cells and FSINs.
(C) Superimposed PC – O-LM (cyan, average of 96 pairs) and PC – FSIN (orange, average of 70 pairs) uEPSCs demonstrate the dramatic difference in the amplitude (the first EPSC is ∼15 times larger in FSINs) and short-term plasticity.
(D) The amplitudes (mean ± SD) of the uEPSCs in O-LM (n = 96 pairs) and FSINs (n = 70 pairs) are shown for the three consecutive APs.
(E) Same as in (D), but normalized amplitude values are shown for demonstration of the difference in the short-term plasticity of the responses.
(F and G) Cumulative probability plots of the peak amplitude of the first uEPSC (F) and the paired-pulse ratio (G) in O-LM cells (cyan) and FSINs (orange). Mean ± SD, coefficient of variations (CV), and number of pairs are shown in the figure. For 17 PC – O-LM pairs, first uEPSC was 0 pA, precluding the calculation of PPR (G).
(H) Same as (A) but in the presence of 1 µM ω-conotoxin to block N-type Ca2+ channels (thin traces: 5 individual pairs; thick trace: the average of 5 PC – O-LM pairs).
(I) Same as (B) but in the presence of 1 µM ω-conotoxin (thin traces: 16 individual pairs; thick trace: the average of 18 PC – FSIN pairs).
(J) Same as (D) but in the presence of 1 µM ω-conotoxin (n = 5 PC – O-LM pairs and n = 18 PC – FSIN pairs, mean ± SD).