Figure 6.

SK2 channel blockers modify theta-burst responses. A, Representative examples of the first (single arrow) and the fourth (double arrows) responses to a train of theta bursts from three groups of slices: control; treated with the SK2 channel toxin apamin (50 nm); and treated with the specific SK2 channel antagonist Lei-Dab⁷ (100 nm). B, Apamin and Lei-Dab⁷ significantly increase the facilitation of burst responses that occur within a theta stimulation train relative to controls (p < 0.01). Shown are the mean ± SEM percentage increases in the areas of the responses to bursts 2–10 relative to the first burst in the train. C, Apamin and Lei-Dab⁷ both reduce the amplitude of the afterpositivity that follows the burst response; measurements were made at 200 msec after the beginning of the theta burst. D, The prolongation of burst responses that occur within a theta train is significantly greater in slices infused with apamin or Lei-Dab⁷ than it is in controls (p < 0.01). The values shown are mean ± SEM percentage changes from the duration of the first burst. E, LTP is enhanced in slices treated with 50 nm apamin or 100 nm Lei-Dab⁷. Graph shows representative experiments evaluating the effects of apamin and Lei-Dab⁷ on LTP. After a train of 10 theta bursts (TBS, upward arrow), the potentiation leveled off at ∼80%, 30 min after LTP induction. This effect is almost double the size of LTP in control slices.F, A single theta burst was applied to slices before and 60 min after treatment with 50 nm apamin or 100 nm Lei-Dab⁷. The percentage change in amplitude (relative to the first field EPSP) of the second, third, and fourth field EPSP within the single theta burst in control, 50 nm apamin-treated, and 100 nm Lei-Dab⁷-treated slices (mean ± SEM) is shown. The magnitude of the individual fEPSPs were no different within pretreatment and posttreatment conditions for both apamin- and Lei-Dab⁷-treated slices.