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Review
. 2001 Nov;24(11):665-70.
doi: 10.1016/s0166-2236(00)01959-7.

Restless AMPA receptors: implications for synaptic transmission and plasticity

C Lüscher  1 , M Frerking
Affiliations
Review

Restless AMPA receptors: implications for synaptic transmission and plasticity

C Lüscher et al. Trends Neurosci. 2001 Nov.

Abstract

A central assumption in neurobiology holds that changes in the strength of individual synapses underlie changes in behavior. This concept is widely accepted in the case of learning and memory where LTP and LTD are the most compelling cellular models. It is therefore of great interest to understand, on a molecular level, how the brain regulates the strength of neuronal connections. We review a large body of evidence in support of the very straightforward regulation of synaptic strength by changing the number of postsynaptic receptors, and discuss the molecular machinery required for insertion and removal of AMPA receptors.

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Figures

Fig. 1
Fig. 1
Model of activity-driven internalization of AMPARs highlighting some unresolved issues. Glutamate (red dots) and insulin (yellow dot) can drive removal of AMPARs from the surface. Increased intracellular Ca2+ [via NMDAR or voltage-gated Ca2+ channel (VGCC)-activation] plays a crucial role in mediating this process, by activating the phosphatase calcineurin. However, some evidence suggests that ligand binding might be sufficient to drive removal on its own. Dephosphorylation of a PKA site near the C terminus of the GluR1 subunit targets internalized AMPARs to the recycling pathway. Conversely, ligand-dependent internalization of AMPARs will not lead to dephosphorylation and as a consequence, the receptors will be degraded in lysosomes. The molecular mechanism as well as the physiological role of insulin-driven internalization remains elusive.
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