Activation of PI3-kinase is required for AMPA receptor insertion during LTP of mEPSCs in cultured hippocampal neurons - PubMed (original) (raw)

. 2003 May 22;38(4):611-24.

doi: 10.1016/s0896-6273(03)00228-9.

Qinhua Wang, Wei-Yang Lu, William Ju, Gholamreza Ahmadian, Lidong Liu, Sandra D'Souza, T P Wong, C Taghibiglou, Jie Lu, Larry E Becker, Lin Pei, Fang Liu, Matthias P Wymann, John F MacDonald, Yu Tian Wang

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Activation of PI3-kinase is required for AMPA receptor insertion during LTP of mEPSCs in cultured hippocampal neurons

Heng-Ye Man et al. Neuron. 2003.

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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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