Fig. 6.
Intra- and extrahippocampus coherence and phase (mean ± SD) as a function of baseline walking and immobility and ketamine dose. (A) Intrahippocampal or distal hippocampus (H1) versus alveus hippocampus (H2), coherence for walking, and immobility conditions during baseline and after ketamine, calculated for different frequency bands: delta (panel 1), theta (panel 2), beta (panel 3), gamma 1 (panel 4, γ1), and gamma 2 (panel 5, γ2). Intrahippocampal delta, gamma 1, and gamma 2 coherence increased, whereas theta and beta coherence decreased, with ketamine dose. (B) Extrahippocampal or alveus hippocampus versus frontal cortex (H2-FC), coherence during baseline and ketamine conditions, plotted as in A. Extrahippocampal (H2-FC) coherence increased with ketamine dose for delta and theta frequency bands but decreased for gamma 1 and gamma 2 bands, mostly opposite the trend of intrahippocampal coherence. (C1) Schematic diagram illustrating recording electrodes in frontal cortex (FC), distal hippocampus (H1), and alveus hippocampus (H2). Gamma oscillations are proposed to be generated by pyramidal cell interacting with interneurons at proximal and distal layers, with entorhinal cortex providing distal excitatory inputs. (C2 and C3) Gamma 1 power at distal hippocampus (C2) and alveus hippocampus (C3) in each group was increased by ketamine. (C4) Mean intrahippocampal (distal vs. alveus hippocampus electrodes, H1–H2) phase, averaged at 50 Hz, was similar across mouse groups during baseline walking (~170o), but forebrain knockout and heterozygous knockdown groups were different from wild-type group after ketamine. (C5) Mean hippocampus alveus versus frontal cortex (H2-FC) phase decreased with ketamine dose, but was not significantly different among the mouse groups. *P < 0.05, knockout versus wild-type; #P < 0.05, knockdown versus wild-type; +P < 0.05, knockdown versus knockout.