Figure 2.

Tetanic stimulation rapidly potentiates DSI of eIPSCs, increases the sensitivity of eIPSCs to CB1 receptor antagonists/inverse agonists, and does not affect the magnitude of DSE. A, B, Tetanic stimulation potentiates DSI of eIPSCs, and the full effect of potentiation is present within 15 min after stimulation. Representative traces are shown in A, summary data are shown in B. Square wave in B represents time and duration of depolarizing pulse. IPSCs were evoked with stimulation at the border of stratum radiatum and stratum pyramidale. DSI was induced by a 500 ms depolarization to 0 mV and recorded in the presence of ionotropic glutamate receptor blockers, but without carbachol. C, In agreement with the lack of change in sIPSC charge transfer after tetanus, the amplitude of evoked IPSCs is not changed by tetanic stimulation for any stimulation intensity tested (note that the stimulating and recording electrodes were carefully positioned in a reproducible manner) (Chen et al., 1999, 2001) (see Materials and Methods). D, Tetanic stimulation potentiates DSI evoked by either 100 or 500 ms depolarizing pulses. E, Tetanic stimulation causes eIPSCs to become sensitive to the CB1 antagonist SR141716. The inset shows representative traces. Calibration: 50 ms, 100 pA. Symbols refer to E and F. F, The potentiation of endocannabinoid signaling caused by tetanic stimulation is specific to inhibitory synapses, as the amplitude and decay of DSE are not affected by tetanus. DSE was evoked by a 10 s depolarizing pulse and was recorded in the presence of bicuculline (10 μm). The square wave represents the time and duration of the depolarizing pulse. The inset shows representative traces. Calibration: 80 ms, 400 pA.