Presynaptic loss of dynamin related protein 1 impairs synaptic vesicle release and recycling at the mouse calyx of held.

This study characterizes the mechanisms underlying defects in synaptic transmission when DRP1 is genetically eliminated. Viral-mediated knockout of DRP1 from the presynaptic terminal at the mouse calyx of Held increased initial release probability, reduced the size of synaptic vesicle recycling pool, and impaired synaptic vesicle recycling. Transmission defects could be partially restored by increasing intracellular calcium buffering capacity with EGTA-AM, implying close coupling of Ca2+ -channels to SVs was compromised. Acute restoration of ATP to physiological levels in the presynaptic terminal did not revert synaptic defects. Loss of DRP1 impairs mitochondrial morphology in the presynaptic terminal, which in turn seems to arrest synaptic maturation. ABSTRACT: Impaired mitochondrial ...

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