Fig. 5. Conditional deletion of Nrxn2 from the hippocampus of adolescent mice enhances the strength of CA3➔CA1 synaptic connections.

(A) Experimental approach. The hippocampal formation of Nrxn2 cKO mice was stereotactically infected at P24 with AAVs expressing inactive (ΔCre, control) or active Cre recombinase (Cre), and mice were analyzed by electrophysiologically and behaviorally 2 to 5 weeks later. (B to E) Conditional Nrxn2 deletion at P24 increases AMPAR-EPSCs elicited by Schaffer collateral stimulation [(B) representative traces of AMPAR-EPSCs induced by increasingly stronger electrical stimulation and recorded at −70 mV in 50 μM picrotoxin and 50 μM D-AP-5 (2R)-amino-5-phosphonopentanoate); (C) input/output plot of the EPSC amplitude versus stimulus strength; (D) slope of the input/output relation; (E) rise and decay times of AMPAR-EPSCs]. (F to I) Conditional Nrxn2 deletion also increases NMDAR-mediated synaptic responses elicited by Schaffer collateral stimulation. Same as (B) to (E), except those responses were recorded at a holding potential of +40 mV in the presence of 20 μM CNQX instead of 50 μM D-AP-5 (2R)-amino-5-phosphonopentanoate). Data are means ± SEM; the numbers of neurons per mice analyzed are listed in the graphs. Statistical assessments were performed by two-way ANOVA (C and G) or Mann-Whitney test (all bar graphs) comparing the Cre condition to the ΔCre controls, with *P < 0.05, **P < 0.01, and ***P < 0.001.