Fig. 3: mGluRII mediates iGC-driven inhibition in mGCs after 10x ECS.
A, B cFos expression in the granule cell layer of the dentate gyrus following rest in the home cage is lower in mice that received 10x ECS vs Sham controls, suggesting that ECS supports a sparser network at rest. C Image of a single confocal plane reveals co-localization of cFos in a DCX+ cell (inset) in the DG of an ECS-treated mouse. DCX was used to identify whether cFos-expressing cells were iGCs (DCX-positive) vs mGCs (DCX-negative). D Within the cFos-expressing population, ECS significantly reduced the proportion of DCX-negative mGCs active at rest in the homecage. E Experimental timeline. Mice received Cort in drinking water for 4 weeks. Six weeks after tamoxifen injection to induce expression of ChR2-EYFP in iGCs, whole-cell recordings were performed in mature granule cells in DG brain slices. Delivery of 10x ECS or Sham occurred one week after tamoxifen-induced Cre recombination. F Breeding strategy and experimental protocol for electrophysiological approach. Nestin-CreERT2 mice were crossed with floxed Channelrhodopsin-EYFP (ChR2-EYFP) expressing mice. Optogenetic stimulation of iGCs evoked responses in mGCs. G We optogenetically stimulated 0-6-week-old iGCs to evoke inhibitory postsynaptic potential in mGCs in the presence of 20 mM NBQX, 50 mM APV, and 20 mM bicuculline (blue trace). These inhibitory signals were blocked by bath application of the mGluRII antagonist APICA (500 mM; gray trace; scale bar = 200 ms, 100 mV). H mGluRII-mediated IPSP had greater negative amplitude after ECS vs Sham in Cort-treated mice. (* p ≤ 0.05, *** p ≤ 0.001).
