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. 2012 Feb 13;7(2):e30402. doi: 10.1371/journal.pone.0030402

Figure 2. XE-991 does not enhance the NMDAR-mediated component of EPSPs.

Figure 2

A) XE-991 (10 µM) depolarised the membrane potential and B) increased input resistance. Example voltage traces show response to a hyperpolarising current in control (black), XE-991 (red), after repolarisation and traces overlaid. Graphs illustrate the timecourse of a single experiment. C) Summated EPSPs during synaptic theta burst stimulation have a small NMDAR-mediated component. Example voltage traces show a burst of five EPSPs under control conditions (black) and in the presence of 50 µM D-AP5 (green). The average normalised decay time constant for a burst of five EPSPs is reduced in the presence of D-AP5. D) XE-991 prolonged the duration of single EPSPs. Example voltage traces in control (black) and XE-991 (red). Average decay time constants increase after application of XE-991. E) XE-991 prolonged the duration of summated EPSPs which was partially reversed either by repolarisation or application of D-AP5. Example voltage traces in control (black), XE-991 (red), XE-991 repolarised (dark red), XE-991 and D-AP5 (green) or XE-991 and D-AP5 repolarised (dark green). Average decay time constants show a partial reversal of EPSP prolongation by D-AP5 at both depolarised and repolarised potentials. F) The effect of D-AP5 on the decay time constant of summated EPSPs was similar in control conditions and in the presence of XE-991. G) XE-991 prolonged the membrane decay time constant in response to a short subthreshold current injection. Example voltage traces in control (black) or XE-991 (red). Average membrane decay time constant shows an increase in XE-991.