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. Author manuscript; available in PMC: 2015 Apr 22.
Published in final edited form as: Brain Res. 2014 Mar 2;1559:11–25. doi: 10.1016/j.brainres.2014.02.043

Fig. 6.

Fig. 6

Effects of NBM-lesions on phase synchronization in frontal cortex, dorsal hippocampus or amygdala. Grand mean values for the phase locking index (PLI) of event-related oscillations in sham operated (black bars), MS-lesion (white bars) and NBM-lesion (gray bars) rats for the rare tone in ROI1 (delta band, 1–4 Hz, 200–500 ms), ROI2 (theta band, 4–7 Hz, 10–400 ms), ROI3 (theta band, 4–7 Hz, 400–800 ms), ROI4 (alpha band, 7–13 Hz, 0–300 ms), ROI5 (alpha band, 7–13 Hz, 300–800 ms), ROI6 (beta band, 13–30 Hz, 0–300 ms), ROI7 (beta band, 13–30 Hz, 300–800 ms), ROI8 (gamma band, 30–50 Hz, 0–300 ms), and ROI9 (gamma band, 30–50 Hz, 300–800 ms). Phase locking index was calculated in: (a) the frontal cortex (Fctx), (b) dorsal hippocampus (DHPC), and (c) amygdala (Amyg). Compared to sham operated rats, MS-lesions (MS les) induced a significant reduction in gamma PLI in Fctx. Compared to sham operated rats NBM-lesion (NBM les) induced a significant reduction in gamma phase locking in Fctx and DHPC and a significant reduction in beta phase locking in Fctx and Amyg and theta phase locking in Fctx. Post-hoc Tukey pairwise comparisons indicate the following: sham vs. NBM-les (*p<0.05) and sham vs. MS-les and NBM-les (**p<0.05).