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Fig. 4. Vglut1 and ZnT3 targeting to AP-3-deficient brain synaptic vesicles. (A) High-speed supernatants (S2) from wild-type (+/+) and mocha (–/–) brain homogenates were fractionated in 5-25% glycerol gradients to resolve small vesicles. Synaptic-vesicle antigen levels across gradients were determined by immunoblot using antibodies against synaptophysin (Sphysin), ZnT3 and Vglut1. ZnT3 and Vglut1 sedimentation patterns and the antigen contents of the membranes were altered in mocha brain vesicles. (B) The normalized content distribution of Vglut1 (n=3). No differences were found in the normalized distribution of synaptophysin (Kantheti et al., 1998; Salazar et al., 2004a). Closed circles represent wild-type membranes, open circles mocha vesicles. (C) The Vglu1 synaptic-vesicle level was determined in the peak fractions. The content of Vglut1 (n=3) was selectively reduced in mocha compared with control brain membranes. No changes were detected in the synaptophysin synaptic-vesicle levels (Kantheti et al., 1998; Salazar et al., 2004a). (D) S2 supernatants were obtained from wild-type (Ap3b2^+/+) and neuronal AP-3-deficient brains (Ap3b2^–/–) and fractionated as described in A. No appreciable differences were observed between brains lacking neuronal AP-3 and brains lacking both neuronal and ubiquitous AP-3 (n=3). ZnT3 synaptic-vesicle levels were partially affected in Ap3b2^–/– (Seong et al., 2005).

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