AD development and synaptic failure in the DG of rat hippocampal slices after 9-min OGD.

<p><b>a</b>. Upper panel: fEPSP taken from a typical experiment at the time-points indicated on the graph in a control hippocampal slice (Ctr) continuously superfused with oxygenated aCSF. Lower panel: example traces taken at the time-points indicated on the graph recorded from a hippocampal slice before (4), at the end of 9-min OGD (5) or 50 min after washout in oxygenated aCSF (6). <b>b</b>. The graph shows the time-course of the fEPSP amplitude, expressed as percent of pre-ischemic baseline in the DG (mean±SEM) in a group of control slices (Ctr, n = 7) or in a group of slices subjected to 9-min OGD (OGD, n = 34). Note that, while a stable fEPSP was recorded in control slices, the ischemic insult elicited a gradual reduction of fEPSPs amplitude, which completely disappears and does not recover even after prolonged washing in oxygenated aCSF. Inset: example traces taken from the same respective hippocampal slices shown in panel <b>a</b>, in control (Ctr, recorded 24 hours from slice preparation) or 24 hours from the end of OGD. In each graph, traces are averages of 3 consecutive responses. Scale bars: 10 ms, 0.5 mV. <b>c</b>. Anoxic depolarization (AD) was recorded as a negative d.c. shift in response to 9-min OGD. The d.c. shift was always recorded (n = 34) during 9-min OGD. <b>d</b>. Each column represents the mean±SEM of AD latency or AD amplitude recorded in the DG during 9-min OGD. AD latency was measured from the beginning of OGD insult.