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Sci. Signal., 24 August 2010
Vol. 3, Issue 136, p. pe28
[DOI: 10.1126/scisignal.3136pe28]

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Bridging the Synaptic Cleft: Lessons from Orphan Glutamate Receptors

Sabine M. Schmid1 and Michael Hollmann2*

1 Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16th Street, GH-N276, San Francisco, CA 94143, USA.
2 Department of Biochemistry I—Receptor Biochemistry, Ruhr-University Bochum, Universitätsstrasse 150, D-44780 Bochum, Germany.

Abstract: For neurons to communicate, signals must cross the cell-to-cell distance at their points of contact. At the predominant cell-cell contact in the central nervous system, the chemical synapse, the synaptic cleft spans roughly 20 nanometers. To signal across this distance, the presynaptic neuron secretes a diffusible neurotransmitter, which is detected by receptors on the postsynaptic neuron. Although this signaling mechanism has become common knowledge, it remains unclear how synapses are maintained when they are not in immediate use. New evidence reveals how Nature solved this problem at a particular type of synapse in the cerebellum: Three old acquaintances bridge the cleft. The ionotropic glutamate receptor GluD2 constitutes the postsynaptic anchor that indirectly interacts with the presynaptic anchor neurexin through a presynaptically secreted soluble factor, a member of the C1q protein family named Cbln1. This trio collaborates to align pre- and postsynaptic sides.

* Corresponding author. E-mail: michael.hollmann{at}ruhr-uni-bochum.de

Citation: S. M. Schmid, M. Hollmann, Bridging the Synaptic Cleft: Lessons from Orphan Glutamate Receptors. Sci. Signal. 3, pe28 (2010).

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