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Activation of PI3-Kinase Is Required for AMPA Receptor Insertion during LTP of mEPSCs in Cultured Hippocampal Neurons

Man, Heng-Ye, Wang, Qinhua, Lu, Wei-Yang, Ju, William, Ahmadian, Gholamreza, Liu, Lidong, D'Souza, Sandra, Wong, T.P, Taghibiglou, C, Lu, Jie, Becker, Larry E, Pei, Lin, Liu, Fang, Wymann, Matthias P, MacDonald, John F, Wang, Yu Tian·2003·Neuron
DOI 10.1016/s0896-6273(03)00228-9
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Abstract

Hippocampal CA1 homosynaptic long-term potentiation (LTP) is expressed specifically at activated synapses. Increased insertion of postsynaptic alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs) appears to be crucial for CA1 LTP. However, the mechanism underlying AMPAR insertion during LTP remains largely unknown. We now report that phosphatidylinositol 3-kinase (PI3K) is complexed with AMPARs at synapses and activated by selective stimulation of synaptic N-methyl-D-aspartate (NMDA) receptors. Activation of the AMPAR-associated PI3K is required for the increased cell surface expression of AMPARs and LTP. Thus, our results strongly suggest that the AMPAR-PI3K complex may constitute a critical molecular signal responsible for AMPAR insertion at activated CA1 synapses during LTP, and consequently, this lipid kinase may serve to determine the polarity of NMDA receptor-dependent synaptic plasticity.

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Metadata

Authors
Man, H.-Y., Wang, Q., Lu, W.-Y., Ju, W., Ahmadian, G., Liu, L., D'Souza, S., Wong, T. P., Taghibiglou, C., Lu, J., Becker, L. E., Pei, L., Liu, F., Wymann, M. P., MacDonald, J. F., & Wang, Y. T.
Venue
Neuron
Publisher
Elsevier BV
Published
2003-05
Volume
38
Issue
4
Pages
611-624
ISSN
0896-6273
DOI
10.1016/s0896-6273(03)00228-9
Cited by
307
References
6
Language
en
Licence
Funders
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (3100-050506.97)
  • EJLB Foundation
  • Heart and Stroke Foundation of British Columbia and Yukon (T-4824)
  • Canadian Institutes of Health Research

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