The molecular basis of CaMKII function in synaptic and behavioural memory

By John E. Lisman, H. Schulman, H. Cline. Nature Reviews Neuroscience, 2002

1,958 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3fe5c2efd3c9d0e4a85136d5745cf29be18d174d

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Citations in the corpus

Long-term potentiation and memory. (2004, result): “A similar conclusion was drawn in experiments that used occlusion to address the question; thus cells that exhibited synaptic potentiation induced by CaMKII were insensitive to tetanic stimulation, and vice versa (335).”
Stable Learning in Stochastic Network States (2012, positive): “The CaMKIImechanismhasbeenprofuselystudiedintheoretical models(Lisman,1989,1994;Lismanetal.,2002;Graupnerand Brunel,2007),showingthatitiswellsuitedtoinducemulti-stabilitystates.”
Experience-dependent structural synaptic plasticity in the mammalian brain (2009, background): “And third, it is impaired in homozygous mice bearing a point mutation (T286A) in the calcium/calmodulin-dependent protein kinase II alpha ( CaMK2a ) gene that abolishes CaMKII autophosphorylatio”
Regulatory mechanisms of AMPA receptors in synaptic plasticity (2007, background): “and is considered an important functional readout for signalling pathways associated with synaptic plasticity and learnin”
Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. (2004, background): “NMDAR-mediated responses are known to regulate the activity, synaptic levels, and localization of CaMKII, which plays a key role in synaptic plasticity (Lisman et al., 2002; Thiagarajan et al., 2002).”
TrkB signalling pathways in LTP and learning (2009, background): “Whereas induction of E-LTP requires transient activation of CaMKII and PKC, maintenance is instead characterized by the persistent activation of these enzyme”
NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII. (2005, neutral): “This LTP requires activation of CaMKII, as KN-93, an inhibitor of CaMKII, blocks potentiation (Figures 1A and 1D; also see Lisman et al., 2002; Zhu et al., 2000).”
A Late-Phase, Long-Term Memory Trace Forms in the γ Neurons of Drosophila Mushroom Bodies after Olfactory Classical Conditioning (2010, background): “A second molecule that has well described roles for mammalian and fly synaptic plasticity and memory is CaMKII (Lisman et al., 2002; Griffith et al., 2003; Elgersma et al., 2004; Griffith, 2004).”
Impact of aging on hippocampal function: plasticity, network dynamics, and cognition. (2003, background): “With more postsynaptic AMPA receptors available, subsequent presynaptic release of glutamate elicits a larger depolarization (for complete reviews, see Malenka and Nicoll, 1999; Luscher et al., 2000; Luscher and Frerking, 2001; Lisman et al., 2002; Malinow and Malenka, 2002).”
ReviewThe Hippocampal-VTA Loop : Controlling the Entry of Information into Long-Term Memory (2005, neutral): “…phosphorylation of CaMKII (Blitzer et al., 1998), a molecule that is necessary and sufficient (in its phosphoryof responses in this pathway proves that the decay of LTP in the tetanized pathway is not simply a result of a lated, active state) for producing LTP (reviewed in Lisman et al., 2002).”