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Updated: Aug 11, 2026

3D Modeling of Dendritic Spines with Synaptic Plasticity
Published on: May 18, 2020
Postsynaptic protein mobility in dendritic spines: long-term regulation by synaptic NMDA receptor activation
Kamal Sharma1, Dan K Fong, Ann Marie Craig
1Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110, USA. ksharma5@jhem.jhmi.edu
Abstract:
Reorganization of molecular components represents a cellular mechanism for synaptic plasticity. Dendritic spines, major sites for glutamatergic synapses, compartmentalize dynamic changes in molecular composition. Here, we use fluorescence recovery after photobleaching (FRAP) in cultured hippocampal neurons to show that spine proteins undergo continual exchange with extra-spine pools. Each spine component has a distinctive mobility: calcium/calmodulin activated protein kinase CaMKIIalpha > GluR1 AMPA glutamate receptor > PSD-95 scaffolding protein > NR1 NMDA glutamate receptor. Stimulation of synaptic NMDA receptors by a protocol that induces chemical LTP resulted in a long-lasting reduction in the mobility of spine CaMKIIalpha and an increased mobile fraction but slower kinetics for spine GluR1. Stimulation also increased the resistance of postsynaptic CaMKIIalpha to detergent extraction. These results suggest long-lasting changes in affinity of protein-protein interactions and/or ongoing alterations in exo/endocytosis. Such lasting changes in protein mobility may contribute to maintaining alterations in synaptic efficacy.
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