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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Trends Neurosci. 2012 Jun 19;35(10):607–618. doi: 10.1016/j.tins.2012.05.003

Table 1.

Manipulations that affect CaMKII function and their effects on hippocampal LTP and learning

(or)
Protein/
residue
Manipulation
(or
modification)
Biochemical effect (of the manipulation
or the native residue)
Hippocampal
LTP
Spatial
Learning
Refs
CaMKIIα Inhibition no activity impaired impaired [5, 27]
KO no α isoform protein impaired impaired [6, 22]
K42 Required for ATP binding N/A N/A
R or M ATP binding impaired impaired impaired [145]
S314 (Phosphorylation) Phos together with T305/306, but unknown function N/A N/A [70, 71]
T253 (Phosphorylation) Phos. enhances PSD association N/A N/A [146]
T286 (Phosphorylation) phos. generates autonomy; fast reaction (~12 sec−1) N/A N/A [2, 29][75]
A no phos.; autonomy impaired impaired impaired [26]
D (regulated overexpression) phos. mimic; constitutively autonomous impaired impaired [147]
T305/306 (Phosphorylation) Phos. prevents stimulation by CaM; slow reaction N/A N/A [70–72]
A/V or A/A no phos.; always stimulatable facilitated impaired “unlearning” [127]
D phos mimic; no stimulation impaired impaired [127]
(β A303R) prevents CaM binding; no stimulation normal normal [89]
CaMKIIβ KO no β isoform protein impaired impaired [89]
GluN2B (T286) L1298A/R1300Q or R1300Q/S1303D impairs CaMKII binding to its major site on GluN2B impaired impaired [93, 94]