Autophosphorylation of αCaMKII Is Required for Ocular Dominance Plasticity
By S. Taha, Jessica L Hanover, Alcino J. Silva, Michael P. Stryker. 2002
114 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f00b8c3801c6345b9665877258bec835b40df85b
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In Cellular and Molecular Neuroscience
In Cognitive Neuroscience
In Molecular Biology
Citations in the corpus
- Synaptic Mechanisms for Plasticity in Neocortex (2009, background): “In V1, rapid ocular dominance plasticity is blocked by several genetic manipulations unrelated to LTD, implicating additional mechanisms in depression of deprived-eye responses (Taha et al. 2002, Yang et al. 2005).”
- Regulation of NMDA Receptor Subunit Expression and Its Implications for LTD, LTP, and Metaplasticity (2008, background): “Because the ocular dominance shift requires the autophosphorylation of CaMKII at threonine 286 (tested by monocular deprivation for 4 days starting at P26-30) (Taha et al., 2002), its expression mechanism shares common molecular pathways with LTP.”
- Hebbian and Homeostatic Plasticity Mechanisms in Regular Spiking and Intrinsic Bursting Cells of Cortical Layer 5 (2015, unknown): “…of CaMKII, and loss of this process in the CaMKII-t286a point mutant (Giese et al., 1998) blocks potentiation of spared whisker responses in layer 2/3 neurons as well as LTP (Hardingham et al., 2003) and disrupts ocular dominance plasticity in the visual cortex (Taha et al., 2002).”
- Tumor necrosis factor-alpha mediates one component of competitive, experience-dependent plasticity in developing visual cortex. (2008, unknown): “While the relationship between ocular dominance plasticity in visual cortex in vivo and LTP/LTD in vitro is not straightforward (Hensch, 2005), they share a number of common features, including dependence on NMDA receptors (Berardi et al., 2003) and its downstream pathways, including calcium calmodu”
- Modeling the dynamic interaction of Hebbian and homeostatic plasticity. (2014, unknown): “…Weakening of the closed eye’s responses is rapid, occur- ring over the first 3 days of MD, and appears to be mediated by Hebbian plasticity because of its dependence on calcium entry through N-methyl-D-aspartate (NMDA) receptors acting on calcium calmodulin kinase type II (Taha et al., 2002).”