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. Author manuscript; available in PMC: 2020 Jan 16.
Published in final edited form as: Neuron. 2018 Dec 3;101(2):246–259.e6. doi: 10.1016/j.neuron.2018.11.018

Figure 7. L. reuteri rescues the impaired social interaction-induced synaptic plasticity in VTA DA neurons of Shank3B−/− mice, but not in mice lacking oxytocin receptors.

Figure 7.

(A) Schematic of electrophysiology experiments.

(B) AMPAR/NMDAR ratio in lateral VTA DA neurons recorded at baseline and 24 hours after reciprocal social interaction (n = 6-8; WT baseline vs. Shank3B−/− + vehicle baseline: t = 1.81, p > 0.99; WT baseline vs. WT social interaction: t = 5.70, p < 0.0001; WT baseline vs. Shank3B−/− + vehicle social interaction: t = 0.29, p > 0.99; WT baseline vs. Shank3B−/− + L. reuteri: t = 1.07, p > 0.99; WT baseline vs. Shank3B−/− + L. reuteri social interaction: t = 4.04, p < 0.01; WT baseline vs. Shank3B−/− + cocaine: t = 3.64, p < 0.05; WT baseline vs. Shank3B−/− + oxytocin social interaction: t = 4.29, p < 0.01; Shank3B−/− baseline + vehicle vs. WT social interaction: t = 7.51, p < 0.0001; Shank3B−/− + vehicle baseline vs. Shank3B−/− + vehicle social interaction: t = 1.58, p > 0.99; Shank3B−/− + vehicle baseline vs. Shank3B−/− + L. reuteri: t = 0.66, p > 0.99, Shank3B−/− + vehicle baseline vs. Shank3B−/− + L. reuteri social interaction: t = 5.78, p < 0.0001; Shank3B−/− + vehicle baseline vs. Shank3B−/− + cocaine: t = 5.38, p < 0.0001; Shank3B−/− + vehicle baseline vs. Shank3B−/− + oxytocin social interaction t = 6.1, p < 0.0001; WT social interaction vs. Shank3B−/− + vehicle social interaction: t = 6.18, p < 0.0001; WT social interaction vs. Shank3B−/− + L. reuteri: t = 6.55, p < 0.0001; WT social interaction vs. Shank3B−/− + L. reuteri social interaction: t = 1.43, p > 0.99; WT social interaction vs. Shank3B−/− + cocaine: t = 1.83, p > 0.99; WT social interaction vs. Shank3B−/− + oxytocin social interaction: t = 1.41, p > 0.99; Shank3B−/− + vehicle social interaction vs. Shank3B−/− + L. reuteri: t = 0.82, p > 0.99; Shank3B−/− + vehicle social interaction vs. Shank3B−/− + L. reuteri social interaction: t = 4.44, p < 0.01; Shank3B−/− + vehicle social interaction vs. Shank3B−/− + cocaine: t = 4.03, p < 0.01; Shank3B−/− + vehicle social interaction vs. Shank3B−/− + oxytocin social interaction: t = 4.72, p < 0.001; Shank3B−/− + L. reuteri vs. Shank3B−/− + L. reuteri social interaction: t = 4.93, p < 0.001; Shank3B−/− + L. reuteri vs. Shank3B−/− + cocaine: t = 4.55, p < 0.01; Shank3B−/− + L. reuteri vs. Shank3B−/− + oxytocin social interaction: t = 5.19, p < 0.001; Shank3B−/− + L. reuteri social interaction vs. Shank3B−/− + cocaine: t = 0.38, p > 0.99; Shank3B−/− + L. reuteri social interaction vs. Shank3B−/− + oxytocin social interaction t = 0.07, p > 0.99; Shank3B−/− + cocaine vs. Shank3B−/− + oxytocin social interaction t = 0.47, p > 0.99; one-way ANOVA F7,46 = 16.68, p < 0.0001). Representative AMPA and NMDA traces are shown above each group.

(C) Reciprocal social interaction was impaired in DA-Oxtr−/− mice and neither L. reuteri or oxytocin reversed the social deficits in these mice (n = 10-12 pairs per group; Controls vs. DA-Oxtr−/− + vehicle: t = 6.095, p < 0.0001; Controls vs. DA-Oxtr−/− + L. reuteri: t = 5.517, p < 0.0001; Controls vs. DA-Oxtr−/− + oxytocin: t = 5.148, p < 0.0001; DA-Oxtr−/− + vehicle vs. DA-Oxtr−/− + L. reuteri: t = 0.6059, p > 0.99; DA-Oxtr−/− + vehicle vs. DA-Oxtr−/− + oxytocin: t = 0.8639, p > 0.99; DA-Oxtr−/− + L. reuteri vs. DA-Oxtr−/− + oxytocin: t = 0.2712, p > 0.99; one-way ANOVA F3,41 = 15.34, p < 0.0001).

(D) AMPA/NMDA ratio of DA neurons in the lateral VTA at baseline and 24 hours after reciprocal social interaction (n = 6-7 per group; DA-Oxtr−/− + vehicle social interaction vs. DA-Oxtr−/− social interaction + L. reuteri: t = 0.02, p > 0.99; DA-Oxtr−/− + vehicle social interaction vs. Controls baseline: t = 0.40, p > 0.99; DA-Oxtr−/− + vehicle social interaction vs. DA-Oxtr−/− + cocaine: t = 5.47, p < 0.0001; DA-Oxtr−/− + vehicle social interaction vs. DA- Oxtr−/− + vehicle: t = 0.44, p > 0.99, DA-Oxtr−/− + vehicle social interaction vs. Controls social interaction: t = 4.92, p < 0.001; DA-Oxtr−/− + vehicle social interaction vs. DA-Oxtr−/− + oxytocin social interaction: t = 0.089, p > 0.99; DA-Oxtr−/− + L. reuteri social interaction vs. Controls baseline: t = 0.37, p > 0.99; DA-Oxtr−/− + L. reuteri social interaction vs. DA- Oxtr−/− + cocaine: t = 5.49, p < 0.0001; DA-Oxtr−/− + L. reuteri social interaction vs. DA-Oxtr−/− + vehicle: t = 0.47, p > 0.99; DA-Oxtr−/− + L. reuteri social interaction vs. Controls social interaction: t = 4.94, p < 0.001; Controls baseline vs. DA-Oxtr−/− + cocaine: t = 6.08, p < 0.0001; Controls baseline vs. DA-Oxtr−/− + vehicle: t = 0.88, p > 0.99; Controls baseline vs. Controls social interaction: t = 5.50, p < 0.0001; Controls baseline vs. DA-Oxtr−/− + oxytocin social interaction: t = 0.32, p > 0.99; DA-Oxtr−/− + cocaine vs. DA-Oxtr−/− + vehicle: t = 5.23, p < 0.001; DA-Oxtr−/− + cocaine vs. Controls social interaction: t = 0.55, p > 0.99; DA-Oxtr−/− + cocaine vs. DA-Oxtr−/− + oxytocin social interaction: t = 5.76, p < 0.0001; DA- Oxtr−/− + vehicle vs. Controls social interaction: t = 4.66, p < 0.001; DA-Oxtr−/− + vehicle vs. DA-Oxtr−/− + oxytocin social interaction: t = 0.55, p > 0.99; Controls social interaction vs. DA-Oxtr−/− + oxytocin social interaction t = 5.19, p < 0.001; one-way ANOVA F6,38 = 13.46, p < 0.0001). ns, not significant. Plots show mean ± SEM. See also Figure S12-S14.