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. Author manuscript; available in PMC: 2014 Jan 1.
Published in final edited form as: Int J Neuropsychopharmacol. 2012 Dec 11;16(6):1309–1318. doi: 10.1017/S1461145712001216

Fig. 3.

Fig. 3

Different modulation of synaptic and extra-synaptic GABAA receptors (GABAAR)-mediated currents: (a) Bath-application of zolpidem (500 nm) showing a decrease of eIPSC amplitude in control animals. The insert shows an example of an evoked inhibitory post-synaptic current (eIPSC) at an expanded scaling control (black) zolpidem (grey). The numbers 1 and 2 in the insert refer to the average of four traces in the amplitude time-course. (b) Same as (a) but in valproic acid (VPA) animals; time-course and traces (insert) showing the effect of zolpidem (500 nm) in eIPSC; control (black), zolpidem (grey). (c) Shows normalized zolpidem-induced change of eIPSC amplitude in control and VPA animals (n=9). (d and e) Change in GABAAR-mediated tonic currents (in 10 μm 6,7-dinitroquinoxaline-2,3-dione and 2 mm kynurenic acid). Examples of time-course of the bath-application of gaboxadol (5 μm), a specific agonist for the extrasynaptic δ subunit of GABAAR, which caused an increase of tonic conductance, revealed by increased holding current blocked by picrotoxin (100 μm), in control and VPA animals, respectively. (f) Mean of picrotoxin sensitive current in gaboxadol normalized to the cell capacitance, control and VPA animals (n=11). * p<0.05.