Skip to main content
. 2008 Oct 1;105(40):15581–15586. doi: 10.1073/pnas.0800621105

Fig. 2.

Fig. 2.

Reduction in release probability and depression but maintenance of synchronous transmitter release at inhibitory BC–GC synapses in synaptotagmin 1-deficient mice. (A) Summary bar graphs of the unitary IPSC amplitude (including failures), percentage of failures, coefficient of variation (CV), and skewness of IPSC peak amplitudes in wild-type (left bar, open circles) and synaptotagmin 1-deficient mice (right bar, filled circles). Bars represent mean values, circles show data from individual experiments. Data are from 22 and 28 pairs, respectively. (B) Onset of multiple-pulse depression of IPSCs during a 50-Hz train of 10 APs. (Upper) Representative average IPSC traces from a wild-type and a knockout synapse. (Lower) Plot of normalized IPSC amplitude (IPSCn/IPSC1) against IPSC number for wild-type (open circles) and knockout (filled circles) synapses. Inset shows measurement of peak amplitude of second and subsequent IPSCs after iterative subtraction of fitted decay phases of preceding IPSCs. Data are from 10 and 12 pairs. (C) (Left) BC–GC IPSCs in reduced Ca2+ to Mg2+ concentration ratio in the bath. Upper traces, presynaptic APs; lower traces, 10 consecutive IPSCs. Average trace is shown in green. (Right) Histogram of first quantal latency (open bars) and corresponding time course of release (filled bars), calculated by using the method of Barrett and Stevens (see SI Text). Data from two pairs (wild-type, Upper; knockout, Lower). Number of events was 151 and 228, respectively; [Ca2+] = 0.5 mM/[Mg2+] = 2.5 mM in wild-type synapses and [Ca2+] = 1 mM/[Mg2+] = 2 mM in knockout synapses to obtain a similar proportion of failures (24% in both cases). (D) Average time course of release. Data were horizontally aligned to the peak release rate for each cell, normalized vertically, and averaged. Data are from five and four pairs. Red curve, single exponential function fitted to the decay.