Fig. 2

The TBOA-induced changes in neuronal hyperactivity depend on the activation of NMDARs at the soma. a–d Time course and magnitude of the change in RMP (a, c) and input resistance (b, d). TFB-TBOA (100 nM) was applied via perfusing the slices (a, b) or via pressure puffing locally on the soma of recorded neurons (c, d). No significant changes in input resistance and RMP were observed after co-application of MK-801 (50 μM) and TFB-TBOA (100 nM). The blue-shaded area indicates the time period of TFB-TBOA treatment. Horizontal bars indicate drug application. The insets illustrate the local application of MK-801 via a pipette placed close to the soma of the recorded neuron. The arrow indicates the timepoint of somatic MK-801 application. e Example traces showing spontaneous firing of recorded CA1 pyramidal neurons before and after co-application of MK-801 and TFB-TBOA. Whole slice perfusion with MK-801 totally abolished the spontaneous firing. f Cumulative distribution of ISIs. g MK-801, when co-applied with TFB-TBOA, reversed the TBOA-induced potentiation in firing rate. h–j Same as in (e–g) except that MK-801 was locally applied on the soma. The duration of local MK-801 application was 500 ms. k Representative samples showing that blockade of GLTs (TFB-TBOA, 100 nM) induced an inward shift in the holding current and local application of MK-801(50 μM) to the soma partially reversed the holding current. l Summary data of the shift of mean holding current. Data are means ± SEM. t test, **P < 0.01