Fig. 9.

A, The mean current–voltage relationship from five outside-out patches excised from CA1 pyramidal cells in hippocampal slices. In each patch, the voltage was ramped between −100 and +30 mV (1–2 sec) between 10 and 50 times in the absence and presence of 50 μm NMDA plus 10 μm glycine. The resulting traces from each patch were averaged together and subtracted; data between patches were subsequently averaged. The box highlights the region analyzed in whole-cell recordings. B, The mean ratio (±SEM) of the whole-cell current–response to pressure-applied NMDA/glycine measured at −70 and at −40 mV is shown before (Pre-treatment) and after 20–30 min of thrombin or buffer treatment. * indicates significantly different from pretreatment (p < 0.05; Wilcoxon rank sum test). C, Plots show increased peak fold potentiation at −70 mV compared with −40 mV for most cells studied (open symbols); a few cells showed larger peak fold potentiation at −40 mV (filled symbols).Squares are data from rat, and circlesare data from mouse. D, The time course (±SEM) of the fold potentiation recorded at both −70 and −40 mV in 19 cells in response to the application of 3 U/ml (30 nm) thrombin.E, The mean peak fold potentiation is shown after PAR1 activation for NR1–1a/NR2B receptors in Xenopus oocytes recorded in the absence of extracellular Mg²⁺. Data are from Figure 7; # indicates p < 0.05 (t test). Solid bars show the mean peak fold potentiation for thrombin-treated hippocampal CA1 pyramidal cells, compared with ACSF-treated cells (Buffer). * indicates significantly different from buffer-treated cells (p < 0.05; Mann–Whitney test); ** indicates significantly different from neuronal results obtained at −40 mV (p < 0.05; Wilcoxon rank sum test).