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The Journal of Neuroscience, November 22, 2006, 26(47):12362-12373; doi:10.1523/JNEUROSCI.3601-06.2006

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Cellular/Molecular
Biophysical Model of AMPA Receptor Trafficking and Its Regulation during Long-Term Potentiation/Long-Term Depression

Berton A. Earnshaw and Paul C. Bressloff

Department of Mathematics, University of Utah, Salt Lake City, Utah 84112

Correspondence should be addressed to Paul C. Bressloff at the above address. Email: bressloff{at}math.utah.edu

AMPA receptors mediate the majority of fast excitatory synaptic transmission in the CNS, and evidence suggests that AMPA receptor trafficking regulates synaptic strength, a phenomenon implicated in learning and memory. There are two major mechanisms of AMPA receptor trafficking: exocytic/endocytic exchange of surface receptors with intracellular receptor pools, and the lateral diffusion or hopping of surface receptors between the postsynaptic density and the surrounding extrasynaptic membrane. In this paper, we present a biophysical model of these trafficking mechanisms under basal conditions and during the expression of long-term potentiation (LTP) and depression (LTD). We show how our model reproduces a wide range of physiological data, and use this to make predictions regarding possible targets of second-messenger pathways activated during the induction phase of LTP/LTD.

Key words: AMPA receptor trafficking; long-term potentiation; long-term depression; synaptic plasticity; exocytosis/endocytosis; membrane diffusion

Received June 13, 2006; revised Sept. 21, 2006; accepted Oct. 19, 2006.

Correspondence should be addressed to Paul C. Bressloff at the above address. Email: bressloff{at}math.utah.edu




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