(A) Schematic drawing of TRPC3 channel function in control (black), gain-of-function (TRPC3Mwk/-, red) and loss-of-function (pcp2Cre;TRPC3fl/fl, green) mice. (B) Schematic approach illustrating of PCs (right circle, dashed lines) recording in vitro, in acute sagittal slices. (C, D) Representative traces of cell-attached PC recordings (top) and corresponding inter spike interval (ISI) distributions (middle) in a Z– PC (left) and a Z+ PC (right) of TRPC3Mwk/- (C) and pcp2Cre;TRPC3fl/fl (D) mice. Z– PCs were affected in TRPC3Mwk/- (C), light-red, n = 15 cells/N = 4 mutant mice vs. n = 15 cells/N = 4 littermate controls, t28 = −2.47, p=0.020 and in pcp2Cre;TRPC3fl/fl mice (D), light-green, n = 40/N = 6 mutants vs. n = 43/N = 5 controls, t81 = 2.69, p=0.009). No differences in the firing rate of Z+ PCs in TRPC3Mwk/- (C), dark-red, n = 13/N = 4 mutants vs. n = 12/N = 4 controls, t18 = 0.419, p=0.680) and pcp2Cre;TRPC3fl/fl mice (D), dark-green, n = 36/N = 10 mutants vs. n = 35/N = 4 controls, t64 = 0.937, p=0.352). (E) Whole-cell patch-clamp recordings in slice from PCs of pcp2Cre;TRPC3fl/fl and control mice were used to test intrinsic excitability, by keeping cells at a holding potential of −65 mV and evoking action potentials by current steps of 100 pA (example, top). Top, exemplary traces evoked by current injection at 600 pA. Bottom, Input-output curves from whole-cell recordings of pcp2Cre;TRPC3fl/fl mice of Z– PCs (left, n = 17/N = 5 mutants vs n = 17/N = 5 controls, t32 = −2.20, p=0.035) and Z+ PCs (right, n = 12/N = 5 mutants vs n = 12/N = 4 controls, t22 = −0.95, p=0.354). gcl, granule cell layer; pcl, Purkinje cell layer; ml, molecular layer. (C–D), data are represented as mean ± s.d.; (E), data are represented as mean ± s.e.m., * means p<0.05 and **p<0.01. For values see Source data.