Skip to main content
. 2002 Feb 1;22(3):654–665. doi: 10.1523/JNEUROSCI.22-03-00654.2002

Fig. 7.

Fig. 7.

Synapsin I and II knock-outs are deficient in the population of RRP. A, Combined results from sequential destaining (as in Fig. 4A) and double-staining experiments (as in Fig. 5A) conducted on 5–7 DIV cultures obtained from mice (395 boutons). Both types of experiments were conducted by using hypertonic solution and high K+ stimulation as described previously.B, Similar experiments performed on synapsin I- and II-deficient synapses (749 boutons) showed a significant reduction in the fraction of vesicles in RRP [Fraction in RRP; 0.20 ± 0.08 (mutant) vs 0.45 ± 0.27 (wild type)]. Mean RP size was not significantly different between mutant and wild-type synapses at this stage [108 (mutant) vs 119 (wild type)F units[. Inset, Cumulative histograms comparing fraction of vesicles in RRP in wild-type and mutant synapses (p < 0.001, Kolmogorov–Smirnov test).C, Distribution of the fraction of vesicles in RRP in wild-type synapses sequentially loaded with FM1-43 (protocol as in Fig.5A). Note the presence of a small number of boutons (11%) with large RRP to RP ratios in a mature population at 22 DIV. The continuous line represents a hyperbolic fit to the distribution of control synapses in which an absolute amount of loading with sucrose was constant at 88 fluorescence units (∼10 vesicles).D, Boutons from synapsin I and II knock-outs had a restricted distribution of RRP/RP ratios ∼0.14 (horizontal line), with a smaller overall RP size as determined by FM1-43 [mean RP size; 501 F units (mutant) vs 646F units (wild type)]. Inset, Cumulative histograms comparing results from wild-type and mutant synapses (p < 0.001, Kolmogorov–Smirnov test).