Distinct modes of endocytotic presynaptic membrane and protein uptake at the calyx of Held terminal of rats and mice.

摘要: Neurotransmitter is released at synapses by fusion of synaptic vesicles with the plasma membrane. To sustain transmission, compensatory retrieval membranes and vesicular proteins essential. We combined capacitance measurements pH-imaging via pH-sensitive protein marker (anti-synaptotagmin2-cypHer5E), compared kinetics calyx Held synapse. Membrane Syt2 were retrieved a similar time course when slow endocytosis was elicited. When fast elicited, still together membrane, but endocytosed organelle re-acidification slowed down, which provides strong evidence for two distinct endocytotic pathways. Strikingly, CaM inhibitors or inhibition Ca(2+)-calmodulin-Munc13-1 signaling pathway only impaired uptake while leaving membrane intact, indicating different recycling mechanisms vesicle proteins. Our data identify novel mechanism stimulus- Ca(2+)-dependent regulation coordinated