Figure 3. Transient depolarization results in a long-term depression of the ADP.

A, traces from a single experiment showing the prolonged (30 min) depression in ADP amplitude following a transient (150 s) depolarization from a holding potential of −84 mV to −14 mV. Calibration: 50 ms, 10 mV. B, pooled data describing the effect of a transient depolarization on ADP amplitude. After obtaining a stable baseline for 10 min, the amplifier was switched to voltage clamp mode and the cell continuously depolarized from −84 mV to −14 mV for 48 s (left; n= 13) or 150 s (right; n= 13). Following the conditioning stimulus, the amplifier was switched back to current clamp mode and the resulting change in ADP monitored for a further 30 min. During current clamp recordings the membrane potential of each cell was maintained close to its initial resting level by automatic somatic current injection, such that the ADP did not initiate a secondary spike. The mean membrane potentials for each data set are plotted at the bottom of each graph (triangular symbols). C, pooled data generated using a similar protocol as described in B. However, in these experiments the cells were depolarized in a phasic, ‘bursting’ pattern, consisting of repetitive depolarizing voltage steps (1 s duration) from −84 mV to −14 mV, repeated either 48 (left; n= 10) or 150 (right; n= 5) times, at 0.5 Hz. D, scatter plot showing the lack of relationship between the resting membrane potential of the neuron and the extent of depolarization-induced plasticity. E, pooled data demonstrating that the extent of depolarization-induced long-term plasticity (measured 30 min after the depolarizing stimulus) is dependent on the duration of depolarization for both phasic (open symbols) and tonic (filled symbols) stimuli. Phasic stimulation for 48 s resulted in a significantly larger depression of the ADP when compared to a continuous depolarization of the same duration (*P < 0.05, unpaired t test).