%0 Journal Article
%T Facilitation of neocortical presynaptic terminal development by NMDA receptor activation
%A Michael P Sceniak
%A Corbett T Berry
%A Shasta L Sabo
%J Neural Development
%D 2012
%I BioMed Central
%R 10.1186/1749-8104-7-8
%X Here, we use confocal imaging to demonstrate that NMDA receptor (NMDAR) activation regulates accumulation of multiple SV and AZ proteins at nascent presynaptic terminals of visual cortical neurons. NMDAR-dependent regulation of presynaptic assembly occurs even at synapses that lack postsynaptic NMDARs. We also provide evidence that this control of presynaptic terminal development is independent of glia.Based on these data, we propose a novel NMDAR-dependent mechanism for control of presynaptic terminal development in excitatory neocortical neurons. Control of presynaptic development by NMDARs could ultimately contribute to activity-dependent development of cortical receptive fields.Synapse formation is a key step in the assembly of the neural circuits that control perception and behavior. In addition, impaired synapse formation may contribute to abnormal development and pathogenesis of neurodevelopmental disorders. Recent genetic and functional studies have linked synapse development to autism spectrum disorders, cognitive impairment, epilepsy, schizophrenia and depression [1,2].During glutamatergic synapse formation in the central nervous system, contact between an axon and a dendrite induces a cascade of events, ultimately resulting in formation of a presynaptic terminal and postsynaptic density at the site of contact. As an integral part of this process, the proteins required for regulated transmitter release must be accumulated at the site of axo-dendritic contact. It has been shown that transport vesicles deliver synaptic vesicle (SV) and active zone (AZ) proteins to developing presynaptic terminals [1,3,4]. Formation of the AZ is then thought to be initiated by fusion of AZ protein transport vesicles with the axonal surface [5]. SVs form within the nascent terminal or are acquired from preassembled clusters of SVs that are mobile within axons [6-9]. As a bouton continues to develop, the number of SVs increases and the AZ expands, requiring continual recruitmen
%U http://www.neuraldevelopment.com/content/7/1/8