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. 2002 Sep 15;22(18):7968–7981. doi: 10.1523/JNEUROSCI.22-18-07968.2002

Fig. 5.

Fig. 5.

Glucosylation of Rac and inhibition of ACh release by LT. A, The substrate specificity of LT82 and LT9048 was determined as described in Figure 3A except thatin vitro glucosylation was performed in the absence or presence of glucosylation competitors: 1 mm unlabeled UDP-mannose (UDP-man.) or 10 mm unlabeled TDP-glucose (TDP-gluc.). The position of molecular weight markers is indicated. B, The ACh release inhibition determined 90 min after injection of LT82 alone (50 nm, final intrasomatic) or together with UDP-mannose (1 mm final) or TDP-glucose (10 mm final), or LT9048 (50 nm final). Data are expressed as a percentage of the average IPSC amplitude determined before injection. Thehorizontal dashed line means no inhibition. Thenumber of experiments in each conditions is indicated. ** denotes significant difference (p < 0.001) as compared with the other conditions. All other comparisons are nonsignificant. C, Same kind of experiment as in Figure2A, except that both presynaptic neurons were injected with LT82 (50 nm, final, white arrow), but one of them (●) was later injected with UDP-mannose (1 mm, final) at the time denoted by theblack arrow (similar results were obtained in 5 experiments).