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. 2021 Apr 22;14:658465. doi: 10.3389/fnmol.2021.658465

Figure 2.

Figure 2

Facilitated excitatory LTP in ventral subicular burst-spiking neurons following acute stress in adulthood. (A) Time course of mean normalized excitatory post synaptic potentials (EPSP) amplitudes at CA1—subiculum synapses to burst-spiking pyramidal neurons. Inset shows sample voltage responses of a subicular bursting neuron to depolarizing (+300 pA) and hyperpolarizing (−300 pA) current pulses. LTP at glutamatergic CA1—subiculum burst-spiking synapses following HFS (arrow, 100 Hz) is enhanced in stressed rats. (B) Quantification of mean normalized EPSP amplitudes (control: n = 6/4, paired Student’s t-test, *p < 0.05; stress: n = 5/4, paired Student’s t-test, *p < 0.05; control vs. stress, unpaired Student’s t-test, *p < 0.05). (C) Attenuated HFS (arrow, 10 pulses at 40 Hz) induces LTP at glutamatergic CA1—subiculum synapses selectively in stressed rats. (D) Quantification of mean normalized EPSP amplitudes (control: n = 6/5, paired Student’s t-test, p = 0.83; stress: n = 8/8, paired Student’s t-test, ***p < 0.001; control vs. stress, unpaired Student’s t-test, ***p < 0.001). (E) Stress experience does not alter basal excitatory synaptic transmission at glutamatergic CA1—subiculum burst-spiking synapses (both n = 6/5; mixed model two-way ANOVA: stimulation strength: F(9,90) = 118.04, p < 0.0001, group: F(1,90) = 0.51, p = 0.49, interaction: F(9,90) = 0.24, p = 0.99). (F) Magnitude of LTP and performance of rats in the active avoidance conditioning test do not correlate (Pearson correlation: r(9) = -0.17, p = 0.63).