The mammalian rod synaptic ribbon is essential for Ca_v channel facilitation and ultrafast synaptic vesicle fusion.

Abstract

Rod photoreceptors (PRs) use ribbon synapses to transmit visual information. To signal 'no light detected' they release glutamate continually to activate post-synaptic receptors. When light is detected glutamate release pauses. How a rod's individual ribbon enables this process was studied here by recording evoked changes in whole-cell membrane capacitance from wild-type and ribbonless (<i>Ribeye</i>-ko) mice. Wild-type rods filled with high (10 mM) or low (0.5 mM) concentrations of the Ca²⁺-buffer EGTA created a readily releasable pool (RRP) of 87 synaptic vesicles (SVs) that emptied as a single kinetic phase with a τ<0.4 ms. The lower concentration of EGTA accelerated Ca_v channel opening and facilitated release kinetics. In contrast, ribbonless rods created a much smaller RRP of 22 SVs, and they lacked Ca_v channel facilitation; however, Ca²⁺ channel-release coupling remained tight. These release deficits caused a sharp attenuation of rod-driven scotopic light responses. We conclude that the synaptic ribbon facilitates Ca²⁺-influx and establishes a large RRP of SVs.