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The Journal of Neuroscience, June 1, 2003, 23(11):4428-4436

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Neocortical Long-Term Potentiation and Experience-Dependent Synaptic Plasticity Require -Calcium/Calmodulin-Dependent Protein Kinase II Autophosphorylation

Neil Hardingham,^1 * Stanislaw Glazewski,^1 * Pavel Pakhotin,^1 * Keiko Mizuno,² Paul F. Chapman,¹ K. Peter Giese,² and Kevin Fox¹

¹ School of Biosciences, Cardiff University, Cardiff CF10 3US, United Kingdom, and ² Wolfson Institute for Biomedical Research, University College London, London WC1E 6BT, United Kingdom

Experience-dependent plasticity can be induced in the barrel cortex by removing all but one whisker, leading to potentiation of the neuronal response to the spared whisker. To determine whether this form of potentiation depends on synaptic plasticity, we studied long-term potentiation (LTP) and sensory-evoked potentials in the barrel cortex of -calcium/calmodulin-dependent protein kinase II (CaMKII)^T286A mutant mice. We studied three different forms of LTP induction: theta-burst stimulation, spike pairing, and postsynaptic depolarization paired with low-frequency presynaptic stimulation. None of these protocols produced LTP in CaMKII^T286A mutant mice, although all three were successful in wild-type mice. To study synaptic plasticity in vivo, we measured sensory-evoked potentials in the barrel cortex and found that single-whisker experience selectively potentiated synaptic responses evoked by sensory stimulation of the spared whisker in wild types but not in CaMKII^T286A mice. These results demonstrate that CaMKII autophosphorylation is required for synaptic plasticity in the neocortex, whether induced by a variety of LTP induction paradigms or by manipulation of sensory experience, thereby strengthening the case that the two forms of plasticity are related.

Key words: barrels; whiskers; LTP; mouse; synapse; plasticity

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Received Jan. 24, 2003; revised Mar. 5, 2003; accepted Mar. 7, 2003.

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