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. 2011 Jul 28;5:63. doi: 10.3389/fnsys.2011.00063

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Copyright © 2011 Jin, Galvan, Wichmann and Smith.

This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

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Tonic activation of presynaptic GABA_BRs induced by GAT-1 blockade in rat brain slices. (A) eIPSCs in response to paired-pulse stimulation (ISI 250 ms) in control solution and in the presence of the GAT-1 blocker, NO-711 (10 μm), in slices of P12-14 rats. Traces represent averages of 20 responses. (B) Quantification of results for NO-711 effects on the mean eIPSC amplitude, PPR (PPR₅₀: ISI 50 ms, PPR₂₅₀: ISI 250 ms), rise time (20–80%) and decay (T_0.10) of striatal eIPSC. Data from 17 striatal output neurons (SONs), except PPR₅₀. (C) Evoked IPSCs in response to paired-pulse stimulation (ISI 250 ms) in control solution and in the presence of either NO-711 or NO-711 plus the GABA_B-receptor antagonist CGP55845 (1 μm). Traces represent averages of 20 responses. (D,E) CGP55845 partially restored the NO-711-induced reduction in eIPSC amplitude and completely reversed the NO-711-induced increase in PPR (ISI 250 ms). ns – not significant, *P < 0.05, **P < 0.01, ***P < 0.001. Reprinted from Kirmse et al. (2008) with permission from John Wiley and Sons.