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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: Neuron. 2017 Nov 1;96(3):697–708. doi: 10.1016/j.neuron.2017.09.056

Figure 2. Astrocytes control synapse formation, maturation and elimination.

Figure 2

A) Astrocytes secrete synaptogenic Thrombospondins (TSP) and hevin, to induce structural synapses, which are presynaptically active but postsynaptically silent due to lack of AMPARs. However, these structural synapses have postsynaptic NMDARs (grey). TSPs induce synapse formation by interacting with their neuronal receptor calcium channel subunit α2δ-1. Hevin induces formation of a subset of excitatory synapses by bridging two interaction-incompatible synaptic receptors, neurexin1-a and neuroligin 1.

B) Astrocyte-secreted glypican 4 induces functional synapse formation by signaling through presynaptic RPTPδ, leading to release of the AMPA receptor clustering factor NP1 from the presynaptic terminal, and binding of NP1 to GluA1 AMPARs (red) on the dendrite.

C) Astrocytes control synapse elimination in two different ways. First astrocytes eliminate unwanted synapses by phagocytosis through the functions of MERTK and MEGF10 receptors. Second, astrocytes release TGFβ, which induces complement protein C1q expression by neurons. C1q is localized to weak/unwanted synapses through an unknown mechanism and recruits microglia, which express complement receptors (CRs) for elimination of these unwanted synapses by phagocytosis.