Esteban et al.
Nat. Neurosci, 6:2, Feb 2003

* PKA phosphorylation of AMPAR subunits contributes to mechanisms underlying plasticity
* state of phosphorylation of GluR1 PKA site: controls channel open time, correlates with changes in synaptic strength
* extensive crosstalk between pathways involved in synaptic plasticity due to enzymes like PKA
* GluR4: PKA can relieve retention
* for GluR4, AMPARs containing GluR4 are incorporated in a manner independent of activity
* PKA activity can induce fast changes in synaptic activity by driving GluR4 incorporation!
* pharmacological activation of PKA leads to increase in CamKII phosphoyrlation of GluR1

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