Fig. 2.
Nerve injury induces activation of gamma-frequency neuronal oscillations in the anterior cingulate cortex. (A) Perfusion with nanomolar concentrations of kainate (150 nM) resulted in the appearance of persistent gamma oscillations. Right, sample traces of kainate-induced gamma oscillations in anterior cingulate cortex slices from sham group and chronic constriction injury (CCI) (days 3 and 7 after surgery) rats. Left, corresponding power spectra of the traces (black, sham group; green, day 3 after CCI surgery; and red, day 7 after CCI surgery.) Scale bars represent 50 μV and 500 ms. (B) Peak frequency from sham group and CCI (days 3 and 7 after surgery) rats. (C) Summary results of the gamma oscillation power from sham group (black, n = 7 slices of four rats), day 3 after CCI surgery (green, n = 7 slices of four rats), and day 7 after CCI surgery (red, n = 8 slices of four rats). **P < 0.01 versus sham group.

Nerve injury induces activation of gamma-frequency neuronal oscillations in the anterior cingulate cortex. (A) Perfusion with nanomolar concentrations of kainate (150 nM) resulted in the appearance of persistent gamma oscillations. Right, sample traces of kainate-induced gamma oscillations in anterior cingulate cortex slices from sham group and chronic constriction injury (CCI) (days 3 and 7 after surgery) rats. Left, corresponding power spectra of the traces (black, sham group; green, day 3 after CCI surgery; and red, day 7 after CCI surgery.) Scale bars represent 50 μV and 500 ms. (B) Peak frequency from sham group and CCI (days 3 and 7 after surgery) rats. (C) Summary results of the gamma oscillation power from sham group (black, n = 7 slices of four rats), day 3 after CCI surgery (green, n = 7 slices of four rats), and day 7 after CCI surgery (red, n = 8 slices of four rats). **P < 0.01 versus sham group.

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