| First Author | Han Y | Year | 2011 |
| Journal | Neuron | Volume | 69 |
| Issue | 2 | Pages | 304-16 |
| PubMed ID | 21262468 | Mgi Jnum | J:250235 |
| Mgi Id | MGI:6099396 | Doi | 10.1016/j.neuron.2010.12.014 |
| Citation | Han Y, et al. (2011) RIM determines Ca(2)+ channel density and vesicle docking at the presynaptic active zone. Neuron 69(2):304-16 |
| abstractText | At presynaptic active zones, neurotransmitter release is initiated by the opening of voltage-gated Ca(2)+ channels close to docked vesicles. The mechanisms that enrich Ca(2)+ channels at active zones are, however, largely unknown, possibly because of the limited presynaptic accessibility of most synapses. Here, we have established a Cre-lox based conditional knockout approach at a presynaptically accessible central nervous system synapse, the calyx of Held, to directly study the functions of RIM proteins. Removal of all RIM1/2 isoforms strongly reduced the presynaptic Ca(2)+ channel density, revealing a role of RIM proteins in Ca(2)+ channel targeting. Removal of RIMs also reduced the readily releasable pool, paralleled by a similar reduction of the number of docked vesicles, and the Ca(2)+ channel-vesicle coupling was decreased. Thus, RIM proteins co-ordinately regulate key functions for fast transmitter release, enabling a high presynaptic Ca(2)+ channel density and vesicle docking at the active zone. |
