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. Author manuscript; available in PMC: 2008 Oct 26.
Published in final edited form as: Neuroscience. 2007 Jul 20;149(2):338–349. doi: 10.1016/j.neuroscience.2007.07.017

Fig. 1.

Fig. 1

Kainate receptor (KAR) activation depressed GABAergic synaptic transmission in the GP. A: time course of the effect of 1 μM KA on GABAA-mediated inhibitory postsynaptic current (IPSC) amplitude (pA) in the presence of 100 μM GYKI 52466 and 50 μM D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5). Three IPSCs are averaged in each trace at the time indicated by the corresponding letters in the graph. B: a summary bar graph showing that KA (0.3–3 μM) significantly reduced the IPSC amplitude and this effect was blocked when 1 μM KA was applied together with 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX) (50 μM). C: time course of the effect of bicuculline (20 μM) on IPSC amplitude in the presence of D-AP5 and CNQX. Three IPSCs are averaged in each trace at the time indicated by corresponding letters in the graph. D: a summary bar graph shows that 20 μM bicuculline completely blocked IPSC amplitude recorded from nine neurons. There was a significant difference from control: * P < 0.001. In this and subsequent figures, “NS” indicates non-significant differences and ‘n’ indicates the number of cells tested under each condition. All averaged data except figure 2, are presented as percent of control ± SEM.