, 2009 and Royer et al., 2010). In contrast, LFP θ in ventral hippocampus would have been an unsuitable reference. LFP θ phase in ventral hippocampus varies dramatically between recordings, preventing a reliable comparison of phase locking find more between animals (Hartwich et al., 2009; Table S6). Moreover, ventral hippocampal θ oscillations have low amplitude and occur only transiently (Adhikari et al., 2010, Hartwich et al., 2009 and Royer et al., 2010), compromising the isolation of θ epochs using unbiased methods

(Csicsvari et al., 1999 and Klausberger et al., 2003) and the calculation of θ phases. To validate that dCA1 signal predicted spike timing of BLA neurons relative to ventral hippocampal θ, we performed BMS-777607 mw experiments that included a vCA1-subiculum electrode (n = 3 animals, 6 neurons). Ventral stratum radiatum LFP signal was used as second reference. Theta oscillations were intermittent and had generally low amplitude, as reported in behaving rodents (Figure S9; Adhikari

et al., 2010 and Royer et al., 2010). As expected, dCA1 signal predicted BLA unit firing modulation with ventral hippocampal θ. Differences between the phases of dCA1 and vCA1-subiculum LFP θ oscillations were similar to, and correlated with the difference between the preferred phases of neuron firing calculated with the two references (Pearson’s correlation r = 0.975, p = 0.025 and circular-circular correlation: Fisher and Lee’s method, Oriana software, p < 0.05, n = 4: 3 principal cells, 1 PV+ basket cell; Figures 7 and S9). Moreover, θ modulation strengths of units calculated with dorsal and ventral hippocampal

references were similar and linearly correlated (Pearson’s correlation r = 0.976, p = 0.024; n = 4; Figure 7D). These results establish that dCA1 is a suitable and sensitive reference to study the coupling of BLA neuron firing to hippocampal θ. This study defines several types of BLA interneurons and their role in shaping BLA activity in relation to dCA1 θ oscillations and noxious stimuli, two Thalidomide processes critical in forming emotional memories. The key findings are the following: dendrite-targeting CB+ interneurons provide inhibition to BLA principal cells in phase with hippocampal θ oscillations. The firing of PV+ basket cells is not tightly synchronized with θ oscillations. Axo-axonic cells consistently and dramatically increase their firing in response to noxious stimuli. In addition, we discovered a GABAergic cell type well placed to coordinate spontaneous and sensory-related BLA-AStria interactions. Our results support the hypothesis that interneurons are critical in regulating timing in the BLA, and that they operate in a cell-type-specific manner. We demonstrate that this principle is not limited to firing relationships with ongoing oscillations, but also applies to the integration of sensory information.