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. Author manuscript; available in PMC: 2012 Dec 29.
Published in final edited form as: Neuroscience. 2011 Oct 19;199:51–63. doi: 10.1016/j.neuroscience.2011.10.015

Figure 3. Acute administration of ketamine and selective NMDAR antagonists potentiates kainate induced gamma oscillations in the PrL cortex.

Figure 3

(A) Left: Field potential records from a representative PrL slice show KA induced gamma oscillations both before and after application of Ketamine (100 µM). Comparing the power spectra of a 5 second epoch of field potential activity recorded after KA application under both conditions, shows a large potentiation of the elicited oscillations and a reduction in the peak frequency. Middle: Field potential records of a representative PrL slice showing KA induced oscillations before and after MK-801 (20 µM) application. Comparing the power spectra of KA elicited activity under each condition shows a large potentiation with MK-801. Right: Field potential records of a representative PrL slice showing KA induced oscillations before and after AP-5 (50 µM) application. Comparing the power spectra of KA elicited activity under each condition shows a large potentiation with AP-5. (B) Bar graphs showing the overall effects of above NMDA antagonists on elicited oscillation across all slices tested. While all agents used significantly potentiated both total gamma power and peak power, only ketamine was observed to have a significant effect on the peak frequency of elicited oscillations. (* p < 0.05; ** p < 0.01)