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Papers In Press, published online ahead of print December 6, 2001
J. Biol. Chem, 10.1074/jbc.M111231200
Submitted on November 26, 2001
Revised on December 6, 2001
Accepted on December 6, 2001

Genetic analysis of aacute;-latrotoxin receptors reveals functional interdependence of CIRL/Latrophilin 1 and neurexin 1á

Sönke Tobaben, Thomas C. Südhof, and Bernd Stahl

Center for Basic Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390

Corresponding Author: Thomas.Sudhof{at}UTSouthwestern.edu

á-Latrotoxin triggers massive neurotransmitter release from nerve terminals by binding to at least two distinct presynaptic receptors, neurexin 1á and CIRL1/ Latrophilin1 (CL1). We have now generated knockout (KO) mice that lack CL1, and analyzed them alone or in combination with neurexin 1á KO mice. Mice lacking only CL1, or both CL1 and neurexin 1á, were viable and fertile. Ca2+-independent binding of á-latrotoxin to brain membranes was impaired similarly in CL1 single and in CL1/neurexin 1á double KO mice (~75% decrease), but not in neurexin 1á single KO mice. In contrast, Ca2+-dependent binding (~2 times above Ca2+-independent binding) was altered in both CL1 (~50% decrease) and neurexin 1á single KO mice (~25% decrease), and decreased further in double KO mice (~75% decrease). Synaptosomes lacking CL1 exhibited the same decrease in á-latrotoxin stimulated glutamate release in the presence and absence of Ca2+ (~75%). In contrast, synaptosomes lacking neurexin 1á exhibited only a small decrease in á-latrotoxin triggered release in absence of Ca2+ (~20%), but a major decrease in the presence of Ca2+ (~75%). Surprisingly, synaptosomes lacking both CL1 and neurexin 1á displayed a relatively smaller decrease in á-latrotoxin stimulated glutamate release than synaptosomes lacking only CL1 in the absence of Ca2+ (~50% vs.~75%), but the same decrease in presence of Ca2+ (~75%). Our data suggest two major conclusions: 1. CL1 and neurexin 1á together account for the majority (75%) of á-latrotoxin receptors in brain, with the remaining receptor activity possibly due to other CL- and neurexin-isoforms. 2. The two receptors act additively in binding á-latrotoxin, but not in triggering release. Together these data suggest that the two receptors act autonomously in binding of á-latrotoxin, but cooperatively in transducing the stimulation of neurotransmitter release by á-latrotoxin.


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