Skip to main content
. 2021 Mar 1;10:e65717. doi: 10.7554/eLife.65717

Figure 6. Retrograde mono-synaptic rabies virus tracing confirms that Lphn3 GPCR activity is essential for Schaffer-collateral synaptic connectivity in vivo.

Figure 6.

(A) Schematic of the experimental approach. The CA1 region of the hippocampus of Lphn3 conditional KO or control mice was injected at P0 with lentiviruses encoding Cre without or with the indicated rescue constructs, at P21 with AAVs encoding Cre-dependent AAVs of rabies-complementing proteins, and at P35 with pseudotyped rabies virus. Mice were analyzed by imaging at P40. (B) Representative images of monosynaptic rabies-virus tracing experiments from the four conditions analyzed. (C) Synaptic connectivity quantifications for the indicated synaptic inputs to CA1 region pyramidal neurons starter cells in the hippocampal CA1 region. Rabies virus tracing demonstrates that the impairment of Schaffer-collateral synaptic connectivity induced by deletion of Lphn3 is rescued by wild-type Lphn3 but not by T4L-mutant Lphn3. Data are means ± SEM (numbers of mice are indicated in bars). Statistical significance was assessed by one-way ANOVA with post hoc Tukey tests for multiple comparisons (For C) (** denotes p<0.01; * denotes p<0.05).

Figure 6—source data 1. Retrograde mono-synaptic rabies virus tracing confirms that Lphn3 GPCR activity is essential for Schaffer-collateral synaptic connectivity in vivo.