Fig. 7
Reciprocal PreL↔IL activity at +12–14 h drives IL function. a, b Impact of inhibiting IL→PreL (a) or PreL→IL (b) projection neurons at +12 h after acquisition on subsequent extinction learning. Repeat measure two-way ANOVA; (a) n = 5 each; Cntrl vs. +12 h, F(1, 4) = 13.63, **P; (b) Cntrl vs. +12 h, F(1, 4) = 19.21, **P. Silencing IL→PreL at +1 h or +16 h after acquisition did not affect subsequent extinction learning (a; n = 5 each; repeat measure two-way ANOVA: +1 h vs. +16 h, F(2, 8) = 1.869, P = 0.197, ns). Sidak’s post hoc test for (a, b). c Local silencing of IL→PreL or PreL→IL projecting axon collaterals in their termination zones at +12 h after acquisition of tFC. Top: schematic of experimental strategy (expression of Neurexin-inhibitory DREADDs fusion protein). Bottom: Suppression of extinction learning by silencing of IL→PreL or PreL→IL collateral terminals in PreL (or IL), but not BLA. Repeat measure two-way ANOVA; n = 5 each; IL→PreL: Inh. PreL vs. BLA, F(2, 8) = 97.73, ***P; PreL→IL: Inh. IL vs. BLA, F(2, 8) = 85.86, ***P. Tukey’s post hoc test for C. d Impact of silencing IL→PreL or PreL→IL projection neurons at +12 h after CD, IDS, or IDSRe learning on subsequent IDS, IDSRe, or EDS learning. Repeat measure two-way ANOVA; n = 5 each; Inh. IL→PreL vs. PreL→IL, F(2, 8) = 36.61, ***P; Tukey’s post hoc. Error bars: SEM; post hoc; P < 0.05 (*), 0.001 (**), 0.0001 (***)
