Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesicles


Wu et al. found that Kv3.3 potassium channels facilitate endocytosis, vesicle mobilization, and recovery of short-term synaptic depression by organizing the presynaptic F-actin cytoskeleton. These “non-conductive” functions are impaired by a Kv3.3 mutation that causes spinocerebellar ataxia. Thus, by nucleating F-actin, Kv3.3 is crucial for endocytosis, synaptic transmission, and neurological disorders.


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