NEUROSCIENCE Correction for “Multiple cannabinoid signaling cascades powerfully suppress recurrent excitation in the hippocampus,” by Kyle R. Jensen, Coralie Berthoux, Kaoutsar Nasrallah, and Pablo E. Castillo, which published January 19, 2021; 10.1073/pnas.2017590118 (Proc. Natl. Acad. Sci. U.S.A. 118, e2017590118).
The authors note that Fig. 1 appeared incorrectly. Symbols in Fig. 1C were swapped by mistake. The corrected figure and its legend appear below.
Fig. 1.
CB1Rs tonically inhibit MC-GC transmission in an input-specific manner. (A) Bath application of the CB1R inverse agonists AM251 (5 μM) and SR141716A (5 μM) reversibly increased MC-GC but not MPP-GC synaptic transmission (pool data; MC-GC 143 ± 6% of baseline, n = 16, P < 0.001, paired t test; MPP-GC 106 ± 4% of baseline, n = 11, P = 0.1, Wilcoxon signed rank test). (Top Left) Recording configuration, (Top Right) representative traces and (Bottom) time-course summary plot. (B) The enhancement of MC-GC transmission by CB1R inverse agonists (AM251 and SR141716A) was accompanied by a significant reduction in PPR (baseline: 1.20 ± 0.05%; CB1R inverse agonist: 0.95 ± 0.04%, n = 12; P < 0.01, Wilcoxon signed rank test) and CV (baseline: 0.19 ± 0.02%; CB1R inverse agonist: 0.13 ± 0.02%, n = 12, P < 0.001, paired t test). (Top) Representative traces and (Bottom) summary plots. (C) AM251-mediated enhancement of MC-GC transmission was absent in Cnr1 cKO mice (Cnr1 cKO: 99 ± 4% of baseline, n = 10; Control: 134 ± 8% of baseline, n = 6; Cnr1 cKO versus Control: P < 0.01, unpaired t test). (Top Left) Representative traces and (Bottom) summary plots. Cnr1fl/fl mice were injected with AAV5.CamKII.mCherry (Control) or AAV5.CamKII.mCherry-Cre (Cnr1 cKO). DSE was virtually abolished in Cnr1 cKO mice as compared to controls (Top Right; Cnr1 cKO: 90 ± 14% of baseline, n = 11; Control: 65 ± 17% of baseline, n = 5; Cnr1 cKO versus Control: P < 0.01, unpaired t test). (D) PPR and CV were reduced in Cnr1 cKO mice as compared to controls (PPR: Control: 1.20 ± 0.08%, n = 8; Cnr1 cKO: 0.82 ± 0.06%, n = 8; Control versus Cnr1 cKO: P < 0.01, unpaired t test; CV: Control: 0.32 ± 0.03%, n = 8; Cnr1 cKO: 0.20 ± 0.02%, n = 8; Control versus Cnr1 cKO: P < 0.05, unpaired t test). (Top) Representative traces and (Bottom) summary plots. (E) Unlike MC inputs, bath application of 5 μM AM251 did not alter IPSCs recruited by stimulating within the IML in the presence of 100 nM DAMGO, 50 μM D-APV, and 10 μM NBQX (101 ± 3% of baseline, n = 8, P = 0.2909, paired t test). These inhibitory inputs expressed robust DSI (Top Right, 63 ± 3% of baseline, n = 8, P < 0.05, Wilcoxon signed rank test). Recording configuration (Top Left): GC; CB1R+ IN, CB1R-sensitive interneuron. (F) AM251 increased MC-GC but not MC-hilar interneuron synaptic transmission. (Top Right) Sample traces showing O-EPSC recorded from GCs and hilar interneurons (INs). (Bottom) A time-course summary plot showing that bath application of AM251 (5 µM) potentiated synaptic transmission at MC-GC synapses (161 ± 13% of baseline, n = 5, P < 0.01, paired t test) but not at MC-INs (93 ± 4% of baseline, n = 5, P = 0.1776, paired t test). O-EPSCs were recorded in the continuous presence of 100 μM picrotoxin. Here and in all figures, data are presented as mean ± SEM; ***P < 0.001; **P < 0.01; *P < 0.05; numbers between brackets indicate the number of recorded cells and animals, and representative traces correspond to the time points indicated by numbers on the time-course plots.