Figure 4.

The sAHP attenuates EPSPs. A, Representative voltage traces showing EPSPs evoked alone (EPSP; blue traces), during the sAHP (AHP; red traces), or during a current injection that simulated the hyperpolarization during the sAHP (HYP + EPSP; green traces). B, Representative EPSPs evoked under control conditions (CTL), during an sAHP (AHP), or during a hyperpolarized current injection have been overlaid. C, Summary data showing the EPSP amplitude normalized to control for each condition. D, EPSPs shown in B replotted normalized to highlight the faster decay of the EPSP during the sAHP. E, Summary data of the decay time constant shows that the EPSPs decay faster when evoked during the sAHP. F, The EPSP decay time constant during the sAHP is plotted against the amplitude of the sAHP immediately before the EPSP. The straight line is the linear regression fit to the data. G, Inclusion of BAPTA in the internal solution abolishes both the sAHP and the shunting of the EPSP after the AP train. The EPSPs under control conditions (blue; CTL) and during the sAHP (red) are shown above the sAHP. H, Application of 10 μm NA reduces both the sAHP and the shunting of the EPSP after the AP train. The EPSPs under control conditions (blue; CTL) and during the sAHP (red) are shown above the sAHP before and after application of noradrenaline. I, Application of the β-adrenergic agonist isoprenaline (10 μm) reduces both the sAHP and the shunting of the EPSP during the sAHP. The EPSPs under control conditions (blue; CTL) and during the sAHP (red) are shown above the sAHP in the presence of the SK channel blocker apamin and during application of isoprenaline (ISO). Summary graphs showing the effect of BAPTA, noradrenaline, apamin, and apamin with isoprenaline on amplitude of the sAHP (J), and the decay (K) of the EPSP during the sAHP. * p < 0.05; ** p < 0.001.