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. 2015 Sep;22(9):461–471. doi: 10.1101/lm.031088.113

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© 2015 O'Dell et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first 12 months after the full-issue publication date (see http://learnmem.cshlp.org/site/misc/terms.xhtml). After 12 months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 2. — Modulation of NMDAR activity mediated by PKA activation downstream from β-AR activation. PKA activation enhances NMDAR activity by phosphorylating sites in the cytoplasmic C-terminal tails of NMDAR GluN1, GluN2A, and GluN2B subunits. In addition, PKA phosphorylates and inhibits Kv4.2 and SK2 type potassium channels present in dendritic spines, thereby enhancing NMDAR activation by facilitating spine depolarization at active synapses.