Figure 7.

Long SB-Spike and SB-Burst Intervals and Extended Time Course of PTP in the Absence of Activity

(A) Left: rasterplot analysis of activity following SBs in GCs in vivo. Points represent activity events (blue, single APs; green, bursts; red, SBs). Events were sorted according to the time point of the last event. Note that the activity extended over several seconds in a subset of events. Inset: summary pie chart of the percentage of SB-single spike (light blue), SB-burst (green), and SB-SB sequences (yellow).

(B and C) Cumulative distributions of latencies between SBs and the first event (B) and last event (C) for all events (black), spikes (blue), and bursts (green). In total, data represent 167 SBs.

(D and E) Similar analysis as shown in (B) and (C) but for the mean latencies in individual GCs. Note that the SB-last event latency covers and occasionally exceeds the time window of PTP. In total, data were obtained from 20 GCs in vivo.

(F) Absence of stimulation extends the time period of PTP. Red, plot of EPSC peak amplitude against experimental time during the standard stimulation paradigm (test stimulation once every 20 s, followed by HFS_100APs, followed by test stimulation once every 20 s); orange, plot of EPSC peak amplitude against time during a stimulation paradigm with a 3- to 4-min delay period. The inset shows test stimulation, and the vertical dashed line indicates HFS_100APs. Note that PTP was significantly larger in the delay protocol than expected for a process that exponentially decays after HFS_100APs. Thus, the time course of PTP was extended in the absence of activity. Data were from 9 pairs (20 s) and 6 pairs (3–4 min).

(G) Comparison of PTP after HFS_100APs, with 20-s delay, 1- to 2-min delay, and 3- to 4-min delay. Data were from 9 pairs (20 s), 6 pairs (1–2 min), and 6 pairs (3–4 min).

In (F and G), PTP was quantified from the amplitudes of the first three EPSCs.

(H and I) Similar plots as in (G) but for RRP (H) and P_r (I). Note that, after a delay, PTP was generated by a selective increase in RRP.

(G–I) Boxes indicate mean values, and error bars denote SEM. ^∗p < 0.05, ^∗∗p < 0.01.

(J) Pool engrams may allow prolonged storage and efficient readout of information in hippocampal circuits. Natural GC activity (SBs) increases the docked vesicle pool, leading to a structural “pool engram.” In the absence of activity (“delay”), the pool engram is long lasting. APs or bursts can lead to readout of information after a delay. The lifetime of the pool engram is limited by the readout (right top) or by the rates of spontaneous release and vesicle undocking (right bottom; Murthy and Stevens, 1999).