Fig. 3

The delayed opening of a sufficient number of NMDARs underlies the ignition of CSD by a threshold stimulus. A NMDAR-dependent component (NMDAR-c) of the neuronal depolarizations elicited by the threshold and just subthreshold KCl stimuli, obtained by subtracting the voltages traces recorded after application of MK-801 to the control voltage traces in the absence of drug (same representative experiment as in Figure 2). Inset: entire CSD voltage change (red trace) and NMDAR-dependent component of the depolarization elicited by the threshold stimulus (blue trace) in a compressed time scale. At CSD threshold stimulation, a large delayed NMDAR-dependent component develops with a delay of 5.8 s from the application of KCl, which is similar to the delay of CSD ignition as derived from the steep IOS rise (5.4 s, cf Figure 2A); the inset shows that this component overlaps with and has the same duration of the CSD depolarization (3^rd peak, cf Figure 1). At just subthreshold stimulation (J-subthr) a delayed NMDAR-dependent component of much smaller amplitude than at threshold, Thr (10 vs 53 mV) develops with a similar delay (5.4 s). B Left: average delay (from the time of the KCl stimulus) of the late NMDAR-c of the depolarization elicited by threshold or slightly suprathreshold KCl stimuli (n = 7; N = 6). Right: average delay from the time of the KCl stimulus of the late NMDAR-dependent component of the depolarization and of the steep IOS rise typical of CSD in 3 experiments in which voltage and IOS were simultaneously recorded in response to threshold KCl stimuli as in the representative experiment in Figure 2