Fig. 2.

Deletion of Gprasp2 impairs glutamatergic transmission. a Input–output curve shows fEPSPs are reduced in the hippocampus of Gprasp2^−/y; WT n = 7/3 slice/mice, KO n = 5/3 slices/mice; two-way repeated measures ANOVA. Inset, representative traces. Scale bar, 0.5 mV, 10 ms. b NP1 amplitude is unaltered between KO and WT littermates; WT n = 7/3 slices/mice, KO n = 5/3 slices/mice. c Paired-pulse facilitation is not altered in Gprasp2 KO mice; WT n = 11/7 slices/mice, KO n = 7/7 slices/mice. Inset shows representative traces. Scale bar, 0.5 mV, 10 ms. d mEPSC traces from Gprasp2^−/y and WT littermates. Scale bar, 10 pA, 1 s. e Representative mEPSC average traces. Scale bar, 5 pA, 10 ms. f, g Reduced mEPSC amplitude (f) but not frequency (g) in Gprasp2^−/y CA1 pyramidal neurons; WT n = 23/4 cells/mice, KO n = 25/4 cells/mice; two-tailed unpaired t-test. h, i Rise (h) and decay (i) times for mEPSCs is unchanged in Gprasp2^−/y and WT mice; WT n = 22/4, KO n = 25/4; two-tailed Mann–Whitney test. j Reduced levels of AMPA receptors and PSD-95 in hippocampal synaptosomal plasma membrane fraction in Gprasp2^−/y mice; WT n = 7–15, KO = 7–13; two-tailed unpaired t-test. Data are presented as means ± s.e.m. Statistical significance: *p < 0.05, **p < 0.01