In neurons, Glycogen Synthase Kinase-3 (GSK-3) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3 present behavioral and cognitive abnormalities, positioning this protein kinase as a key signaling molecule in normal brain functioning. Furthermore, mouse models with defective GSK-3 activity display distinct structural and behavioral abnormalities, which model some aspects of different neurological and neuropsychiatric disorders.
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