Figure 8.

Rab3a deletion does not affect spontaneous synaptic activity but inhibits EPSC enhancement produced by either 4-AP application or increased extracellular Ca²⁺. A, Recordings of sEPSCs (inward) and sIPSCs (outward) activity in the absence of blockers at −50 mV holding potential in WT and Rab3a(−) slices derived from young mice. B, sEPSC amplitude histograms for WT and Rab3a(−) synapses. No significant shift in the sEPSC amplitude in Rab3a(−) synapses was detected (p = 0.5 per Kolmogorov–Smirnov test). C, Cumulative plot for the sEPSC interevent interval recorded in WT and Rab3a(−) slices. The interevent interval is slightly increased in Rab3a(−) synapses, but this effect is not statistically significant (p = 0.16 per Kolmogorov–Smirnov test). B, C, Histograms represent results from all the experiments pooled together for each genotype. Data were collected from 7 Rab3a(−) cells (4 mice). WT data (dotted lines) are replotted from Figures 1 and 2. D, 4-AP elicits a significant enhancement in the sEPSC frequency in Rab3a(−) synapses (p = 0.028, n = 7) This affect appears to be weaker than in WT synapses, although the difference between the phenotypes is not significant (p = 0.22). E, In Rab3a neurons, administration of 4-AP (10 μm) fails to produce any detectable change in EPSC amplitude (E₁,E₃, p = 0.425, n = 7), whereas it elicits a significant increase in IPSC amplitude (E₂,E₃, p = 0.010, n = 7). E₃, The effect of 4-AP on EPSCs and IPSCs in the two genotypes. F, In Rab3a neurons, elevating extracellular calcium fails to produce a statistically significant change in EPSC amplitude (F₁, p = 0.10, n = 7), whereas it elicits a significant increase in IPSC amplitude (F₂, p = 0.05, n = 6). F₃, The effect of elevated calcium on EPSCs and IPSCs in the two genotypes. The effect of 4-AP was quantified as the ratio between EPSC or IPSC amplitudes after and before treatment. Data were collected from 4 mice. Fifty responses at each condition were collected in each experiment.