Eye opening and PSD95 are required for long-term potentiation in developing superior colliculus
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Zhao-2012-Eye opening and PSD9.pdf
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2.48 MB
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Author(s)
Zhao, Jian-Ping
Murata, Yasunobu
Constantine-Paton, Martha
Date Issued
December 2012
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Zhao, J.-P., Y. Murata, and M. Constantine-Paton. Eye Opening and PSD95 Are Required for Long-term Potentiation in Developing Superior Colliculus. Proceedings of the National Academy of Sciences 110, no. 2 (January 8, 2013): 707-712.
Version
Final published version
Abstract
The only major glutamate receptor membrane-associated guanylate kinase scaffolds expressed in the young superficial superior colliculus (SC) are synapse-associated protein 102 (SAP102) and postsynaptic density protein 95 (PSD95). In this, as in all visual brain regions examined, synaptic PSD95 increases rapidly following simultaneous eyelid opening (EO). We show that EO and PSD95 are necessary for SC NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) and this LTP is eliminated or reinstated by manipulating EO. PSD95 knockdown (KD) in vivo blocks this LTP, but not long-term depression, and reduces frequencies of miniature AMPA receptor and NMDAR currents with no change in presynaptic release. Furthermore, miniature NMDAR currents after PSD95 KD show an activity-triggered calcineurin sensitivity that is normally only found in the pre-EO period when SAP102 binds mixed GluN2A/GluN2B NMDARs. These data indicate that young SC LTP arises from PSD95 unsilencing of silent synapses, that unsilencing is labile in young brain, and that even though SAP102 and PSD95 can bind the same NMDARs, only PSD95 enables SC synaptic maturation.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
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DOI of Published Version
https://doi.org/10.1073/pnas.1215854110
