Figure 6.
NemobeKO mice show signs of reduced sensory adaption accompanied by a decreased number of somatostatin (SOM) positive neurons. (A) Representative whisker-evoked neuronal responses (first peaks average, 8 Hz, 20 s stimulation) over the barrel cortex. (B) P1-N1 amplitude example traces and quantifications of first peak showed a trend for NemobeKO mice to have higher amplitude as compared to NemoFl controls with an 8 Hz whisker stimulation frequency. (C) Representative stimulation trains of an 8 Hz stimulation for 20 s. (D) Quantification of peak amplitude average over 20 s stimulation train showed larger responses in NemobeKO mice (p < 0.05), with similar trends at each 5 s segment over the entire stimulation period. (E) When electrophysiological responses were separated into different frequency bands no group differences were observed. N = 8/group. Unpaired samples t-tests were used to compare NemobeKO and NemoFl groups for electrophysiology experiments. There was a loss of SOM positive neurons in the barrel cortex of NemobeKO mice that was not observed in the NemobeKO mice that exercised (EX) or were treated with simvastatin (SV), and this loss was not seen in the recovery cohort following 3 months off tamoxifen (F). In contrast, no differences in parvalbumin- (PV, G) or cholecystokinin- (CCK, H) containing cortical interneurons in the barrel cortex were observed. There was a significant decrease in the number of choline acetyltransferase (ChAT) positive neurons in the basal forebrain of NemobeKO mice that was slightly improved by SV and fully protected by EX, and which returned to NemoFl levels in the recovery cohort (I). N = 4–5 mice/group and one-way ANOVA with post-hoc Newman-Keuls multiple comparison tests were performed for immunohistochemistry analysis *p < 0.05, **p < 0.01, ***p <.001.