Astrocyte glypican 5 regulates synapse maturation and stabilization. Bosworth, A., Contreras, M, Novak, S W., Sancho, L, Salas, I., Manor, U, & Allen, N. bioRxiv, Cold Spring Harbor Laboratory, 2023. ![Astrocyte glypican 5 regulates synapse maturation and stabilization [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex The maturation and stabilization of appropriate synaptic connections is a vital step in the development of neuronal circuits, however the molecular signals underlying these processes are not fully understood. We show that astrocytes, through production of glypican 5 (GPC5), are required for maturation and refinement of synapses in the developing mouse cortex. In the absence of astrocyte GPC5 thalamocortical synapses in the visual cortex show structural immaturity during the critical period, including smaller presynaptic terminals, decreased postsynaptic density area, and presence of more postsynaptic partners at multisynaptic connections. This structural immaturity is accompanied by a delay in developmental incorporation of GLUA2-containing calcium impermeable AMPARs at intracortical synapses. The functional impact of this is that mice lacking astrocyte GPC5 exhibit increased levels of ocular dominance plasticity in adulthood. This shows astrocyte GPC5 is necessary for maturation and stabilization of synaptic connections in typical development, with implications for understanding disorders with altered synaptic function, including Alzheimer\textquoterights disease, where GPC5 levels are altered.Competing Interest StatementThe authors have declared no competing interest.
@article {Bosworth2023.03.02.529949,
author = {AP Bosworth and M Contreras and S Weiser Novak and L Sancho and IH Salas and U Manor and NJ Allen},
title = {Astrocyte glypican 5 regulates synapse maturation and stabilization},
elocation-id = {2023.03.02.529949},
year = {2023},
doi = {10.1101/2023.03.02.529949},
publisher = {Cold Spring Harbor Laboratory},
abstract = {The maturation and stabilization of appropriate synaptic connections is a vital step in the development of neuronal circuits, however the molecular signals underlying these processes are not fully understood. We show that astrocytes, through production of glypican 5 (GPC5), are required for maturation and refinement of synapses in the developing mouse cortex. In the absence of astrocyte GPC5 thalamocortical synapses in the visual cortex show structural immaturity during the critical period, including smaller presynaptic terminals, decreased postsynaptic density area, and presence of more postsynaptic partners at multisynaptic connections. This structural immaturity is accompanied by a delay in developmental incorporation of GLUA2-containing calcium impermeable AMPARs at intracortical synapses. The functional impact of this is that mice lacking astrocyte GPC5 exhibit increased levels of ocular dominance plasticity in adulthood. This shows astrocyte GPC5 is necessary for maturation and stabilization of synaptic connections in typical development, with implications for understanding disorders with altered synaptic function, including Alzheimer{\textquoteright}s disease, where GPC5 levels are altered.Competing Interest StatementThe authors have declared no competing interest.},
URL = {https://www.biorxiv.org/content/early/2023/03/02/2023.03.02.529949},
eprint = {https://www.biorxiv.org/content/early/2023/03/02/2023.03.02.529949.full.pdf},
journal = {bioRxiv}
}
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We show that astrocytes, through production of glypican 5 (GPC5), are required for maturation and refinement of synapses in the developing mouse cortex. In the absence of astrocyte GPC5 thalamocortical synapses in the visual cortex show structural immaturity during the critical period, including smaller presynaptic terminals, decreased postsynaptic density area, and presence of more postsynaptic partners at multisynaptic connections. This structural immaturity is accompanied by a delay in developmental incorporation of GLUA2-containing calcium impermeable AMPARs at intracortical synapses. The functional impact of this is that mice lacking astrocyte GPC5 exhibit increased levels of ocular dominance plasticity in adulthood. 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