Figure 1.

Increased neuronal activity leads to potentiation of DSI. A, B, Strong (5 × 10 s at 100 Hz) tetanic stimulation in the stratum radiatum (including the Schaffer collateral pathway) in slices from control animals increased DSI amplitude and prolonged the DSI decay in CA1 pyramidal cells. Example traces are shown in A; summary data are shown in B (based on 3 DSI episodes per cell separated by 1 min). Square waves above traces and summary graph indicate time and duration of depolarization. C, Even after tetanic stimulation, DSI is completely blocked in the presence of the CB1 receptor antagonist SR141716 (1 μm). D, Tetanic stimulation and hyperthermic seizures (performed 1 week before recording), both potentiate DSI to a similar extent. Additionally, tetanic stimulation cannot further potentiate DSI in slices from HT animals, suggesting a common mechanism of potentiation. E, The potentiation of DSI requires a strong tetanic stimulation, as a weaker protocol (5 × 1 s at 100 Hz) does not increase DSI. For all experiments in this figure, DSI was induced by a 500 ms depolarization to 0 mV and recorded in the presence of carbachol and ionotropic glutamate receptor blockers (see Materials and Methods). Recordings were made at least 1 h after sham stimulation (sham-tet) or tetanus (tetanus). In this and following figures, asterisks indicate significant differences (p < 0.05).