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. 2013 Nov 11;203(3):395–405. doi: 10.1083/jcb.201306099

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© 2013 Corty and Freeman

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 3. — Model of astrocyte–neuron interactions during synapse formation and maturation. (A) Astrocytes secrete several factors to promote structural synapse formation. Astrocytes secrete thrombospondins (TSPs), which act through α2–δ1 calcium channel subunit/gabapentin receptors to drive formation of structurally intact glutamatergic synapses. The exact mechanism by which TSP binding to α2–δ1 promotes adhesion and structural synapse formation is unknown. Astrocytes also secrete hevin and SPARC. Hevin also promotes structural synapse formation, whereas SPARC antagonizes this function. Competition between hevin and SPARC for a common unknown binding partner on neurons may explain the antagonism. The synapses formed in response to TSPs or hevin are structurally intact with docked vesicles and PSD-95 correctly localized; however, they lack surface expression of AMPARs at the postsynapse and are therefore not fully functional. (B) Other astrocyte-secreted factors influence surface expression and clustering of glutamatergic AMPARs. Glypicans secreted from astrocytes act through an unidentified receptor to promote surface expression and clustering of AMPARs during development. Activity can also induce astrocytes to secrete SPARC, which can perturb integrin interactions with surface AMPARs, leading to decreased surface expression of AMPARs in response to excess activity.