Our system uses c-fos-tTA transgenic mice, in which the promoter of the c-fos gene drives the expression of the tetracycline transactivator (tTA) to induce expression of a gene of interest downstream of the tetracycline-responsive element (TRE) (8–12). We injected an adeno-associated virus (AAV) encoding TRE-ChR2-mCherry into the DG or CA1 of c-fos-tTA animals (Fig. 1A). Channelrhodopsin-2 (ChR2)–mCherry expression was completely absent in the DG of animals that had been raised with doxycycline (Dox) in the diet (on Dox) (Fig. 1B). Exploration of a novel context under the condition of Dox withdrawal (off Dox) elicited an increase in ChR2-mCherry expression (Fig. 1C). We confirmed the functionality of the expressed ChR2-mCherry by recording light-induced spikes in cells expressing ChR2-mCherry from both acute hippocampal slices and in anaesthetized animals (Fig. 1, D to F). Furthermore, optical stimulation of ChR2-mCherry–expressing DG cells induced cFos expression throughout the anterior-posterior axis of the DG (fig. S1, A to I).
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Absalom, Absalom! 