Fig. 2: Synaptic excitatory transmission is increased in Glu-CB1-KO.

a, h Schematic drawings and infrared differential interference contrast images showing the recorded neuron in the a PL and h NAc. Scale bars, 30 µm. b, e Representative traces of miniature excitatory and inhibitory postsynaptic currents (mEPSCs, mIPSCs) recorded at a holding potential of −70 mV in PL and i, l −75 mV in NAc from WT (black traces) and Glu-CB1-KO (blue traces) mice. c, d mEPSCs frequency and amplitude and f, g mIPSCs frequency and amplitude of WT and Glu-CB1-KO mice in the PL and j, k, m, n in the NAc (mean ± S.E.M; t-test, *P < 0.05, **P < 0.01, n = 9–12 cells from n = 12 mice). o–p Paired pulse facilitation (PPF). o Representative recordings of L5 field postsynaptic potentials (fPSPs) before (P1) and after (P2) stimulating twice in layer 2/3 with an interpulse interval of 50 ms for WT (above) and Glu-CB1-KO (below). p Increased paired-pulse facilitation ratio (P2/P1) in Glu-CB1-KO compared to WT (mean ± S.E.M, U Mann–Whitney, **P < 0.01; n = 12–14 slices from  n = 5 animals per genotype). q Representative recordings of the modulation of fPSPs amplitude before and after application of the CB₁R agonist WIN55,212-2 (5 µM) compared to baseline in PL for WT (above) and Glu-CB1-KO (below). r Changes of fPSPs amplitude in percentage in PL for WT and Glu-CB1-KO (mean and individual values, paired t-test, ***P < 0.001; n = 6 slices from n = 3 animals per genotype). s Representative synaptic responses showing mean EPSCs (five consecutive EPSCs) before and after CB₁R agonist WIN55,212-2 (5 µM) bath application in the NAc for WT (above) and Glu-CB1-KO (below). t Average relative changes of EPSCs amplitude in NAc of WT and Glu-CB1-KO mice (mean and individual values, paired t-test, **P < 0.01, ***P < 0.001; n = 7–10 cells from n = 4 animals per genotype; see also Supplementary Fig. 3; statistical details are included in Supplementary Table 2).