Dysbindin links presynaptic proteasome function to homeostatic recruitment of low release probability vesicles.

ABSTRACT: Here we explore the relationship between presynaptic homeostatic plasticity and proteasome function at the Drosophila neuromuscular junction. First, we demonstrate that the induction of homeostatic plasticity is blocked after presynaptic proteasome perturbation. Proteasome inhibition potentiates release under baseline conditions but not during homeostatic plasticity, suggesting that proteasomal degradation and homeostatic plasticity modulate a common pool of vesicles. The vesicles that are regulated by proteasome function and recruited during homeostatic plasticity are highly EGTA sensitive, implying looser Ca²⁺ influx-release coupling. Similar to homeostatic plasticity, proteasome perturbation enhances presynaptic Ca²⁺ influx, readily-releasable vesicle pool size, an

SUBMITTER: Wentzel C 

PROVIDER: S-EPMC5773495 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature