Extended Data Fig. 10: Chemogenetic inhibition of PV + or SOM + interneurons does not alter spatial coding in CA1.

a. To selectively inhibit PV + and SOM + interneurons, we used PV-Cre and SOM-Cre mice and injected a cre-dependent virus expressing hM4Di (AAV5-Syn-DIO-hM4Di-mCherry) or control virus (AAV5-Syn-DIO-mCherry). We also injected virus to express GCaMP6f in all neurons (AAV1-Syn-GCaMP6f) to allow for calcium imaging. We then trained mice to run on a linear track and delivered CNO (5 mg/kg) or Vehicle (VEH) 45 min prior to imaging on the track. b. To confirm that CNO was effective in reducing firing in vitro we used whole-cell recordings of hippocampal mCherry + interneurons in acute brain slices and applied ACSF or ACSF with CNO during stimulation. Interneurons expressing hM4Di had reduced spiking to stimulation (middle, right) while control virus did not reduce spiking. c. We found no differences in information content between VEH and CNO in any of the groups examined (Paired t-tests – PV: t(4) = 1.769, P = 0.15; SOM: t(3) = 0.717, P = 0.53). d. We found no differences in stability between VEH and CNO in any of the groups examined (Paired t-tests – PV: t(4) = 2.047, P = 0.11; SOM: t(3) = 0.672, P = 0.55). e. We found no differences in place cell percent between VEH and CNO in any of the groups examined (Paired t-tests – PV: t(4) = 2.29, P = 0.08; SOM: t(3) = 0.169, P = 0.88). f. We found increased Activity with CNO compared to VEH in the PV-hM4Di mice, but not SOM mice (Paired t-tests – PV: t(4) = 2.897, P = 0.04; SOM: t(3) = 0.96, P = 0.41). N = 2 PV-Cre mCherry animals, N = 4 SOM-Cre hM4Di animals, N = 5 PV-Cre hM4Di animals. Error bars denote 1 S.E.M. *P < 0.05.