Eight double recording experiments were performed, in which we recorded simultaneously from a dorsal and a more ventrally located site along the MEC axis (average distance between recording locations = 1.44 ± 0.14 mm). Recordings were targeted to L1, where gamma power is known to be highest (Quilichini et al., 2010; Figures 7E and 7F; see Experimental Procedures). Dorsal and ventral recording sites were located at a similar distance from the pial surface (dorsal recordings:
124.3 ± 10.97 μm; ventral recordings: 96.38 ± 20.84; p = 0.13; paired t test, see also Figure S3B). During periods of theta oscillatory activity (4–12 Hz, see Experimental Procedures), the PSD integral of gamma oscillations (30–100 Hz) was indeed significantly Lapatinib cell line smaller in ventral recording locations compared to dorsal recording locations (dorsal: 0.669 ± 0.096 ×10−3 mV2, n = 8; ventral: 0.293 ± 0.048 ×10−3 mV2, n = 8; p < 0.01, paired
t test; Figure 7G). We also observed a linear correlation between size of the PSD integral and distance from the dorsal MEC border (r2 = 0.403; p < 0.01; Figure 7H), suggesting that gamma power might progressively decrease along the dorsoventral MEC axis. In summary, we could show that gamma oscillations, which depend on the inhibitory microcircuitry, are altered along the dorsoventral axis of buy Romidepsin the medial entorhinal cortex, both in in vitro and in vivo conditions. This difference in the power of gamma oscillations may have a functional impact on the computational
working principles at different locations of the entorhinal network. In this study, we describe a strong inhibitory network that impinges on layer II stellate cells in the medial entorhinal cortex, which is Oxalosuccinic acid reported to contain spatially modulated cells (Hafting et al., 2005). This strong inhibition is characteristically different from a similar cell type in the lateral part of the entorhinal cortex that contains no spatially modulated cells. Here, we investigate the role of this inhibitory microcircuit onto the L2S. Using a combination of different electrophysiological and optical approaches, we found a finer structure to this microcircuitry, namely, that there is a strongly decreasing gradient of inhibition along the dorsoventral axis in the MEC. Additionally, we describe that this dense inhibitory circuitry onto the L2S in the entorhinal cortex is mostly mediated by parvalbumin positive (PV+) interneurons. It is not the number of PV+ interneurons that decrease along the dorsoventral axis but rather the number of synaptic contacts made onto a postsynaptic L2S in the MEC. However, a colabeling with V-GAT showed that GABAergic terminals remained unchanged along this axis. This suggests a complementary increase in other subpopulations of interneurons as reported earlier by Fujimaru and Kosaka (1996).