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Modulation of GABA A receptor function and inhibitory synaptic transmission by phosphorylation has profound consequences for the control of synaptic plasticity and network excitability. We have established that activating ␣-calcium/calmodulin-dependent protein kinase II (␣-CaMK-II) in cerebellar granule neurons differentially affects populations of IPSCs that correspond to GABA A receptors containing different subtypes of ␤ subunit. By using transgenic mice, we ascertained that ␣-CaMK-IIdoi:10.1523/jneurosci.5531-07.2008 pmid:18650335 fatcat:afpaiporkncc3g4l2r7l2g52zm