Abstract
Anatomical and electrophysiological experiments1,2,3,4,5,6 show that central excitatory synapses initially display NMDA (N-methyl-d-aspartate) receptors (NMDARs) and subsequently mature by acquiring AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors (AMPARs). NMDAR activation can lead to rapid synaptic delivery of AMPARs ('AMPAfication')7,8, but the view that AMPAfication during development requires NMDAR activation has been challenged by studies showing that chronic removal of NMDAR function (either genetically9,10 or pharmacologically11,12,13,14) has no apparent effect on acquisition of AMPAR-mediated synaptic transmission. Here we show that NMDARs are crucial in the developmental acquisition of AMPAR-mediated synaptic transmission, and that chronic disabling of NMDAR function triggers compensatory mechanisms for NMDAR-independent AMPAfication.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
