P-Rex-deficient Purkinje neurons have normal passive membrane properties and basal synaptic transmission.

A) Rise time and decay time of EPSC (measured between 10–90% of amplitude as indicated), and paired pulse ratio of amplitude are indistinguishable in Purkinje neurons from WT (n = 13) and P-Rex dKO (n = 12) mice. B) Relationship between stimulus strength and EPSC amplitude in cells from WT (n = 10) and P-Rex dKO (n = 10) mice. C) Slow EPSCs recorded in response to 10 stimuli at 100 Hz in cells from WT (black trace) and P-Rex dKO (grey trace) mice. Slices were preincubated with 10 µM NBQX to inhibit fast AMPAR currents. Slow current is inhibited by the mGluR antagonist CPCCOEt (20 µM; red trace). Aggregate data shows mean ± s.e.m. amplitude of sEPSC in WT (n = 6) and P-Rex dKO (n = 7) cells, in response to 2, 5 or 10 pulses at 100 Hz. D) Current decay after 10 mV depolarizing step (−80 to −70 mV) in representative WT (black trace) and P-Rex dKO (grey trace) cells. Currents are well fitted by biexponential curves (red lines). Aggregate data show no differences in steady-state currents, nor time constants or areas of either exponential phase (n = 6 WT cells; n = 7 P-Rex dKO cells). E) Representative current traces recorded from Purkinje neurons during pressure ejection of s-AMPA (100 µM) onto the molecular layer (dendrites) or cell somata (soma) of slices from WT and P-Rex dKO mice. Aggregate data show no differences in mean ± s.e.m. amplitudes between genotypes (n = 9 WT and 11 P-Rex dKO cells). F) Loose cell-attached recordings of spontaneous action potential firing in representative Purkinje cells from WT and P-Rex dKO mice. Aggregate data show no differences in mean ± s.e.m. for n = 29 cells each.