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Activity-dependent rapid structural and functional modifications of central excitatory synapses contribute to synapse maturation, experience-dependent plasticity, and learning and memory and are associated with neurodevelopmental and psychiatric disorders. However, the signal transduction mechanisms that link glutamate receptor activation to intracellular effectors that accomplish structural and functional plasticity are not well understood. Here we report that NMDA receptor activation in pyramidal neurons causes CaMKII-dependent phosphorylation of the guanine-nucleotide exchange factor (GEF) kalirin-7 at residue threonine 95, regulating its GEF activity, leading to activation of small GTPase Rac1 and rapid enlargement of existing spines. Kalirin-7 also interacts with AMPA receptors and controls their synaptic expression. By demonstrating that kalirin expression and spine localization are required for activity-dependent spine enlargement and enhancement of AMPAR-mediated synaptic transmission, our study identifies a signaling pathway that controls structural and functional spine plasticity.
Pubmed ID: 18031682 RIS Download
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Software tool that detects peaks of any type, any shape, any direction, and any size for neuroscientists who are studying spontaneous activities. Allows detection of virtually any kind of peaks including spontaneous miniature synaptic currents and potentials, action potential spikes, calcium imaging peaks, amperometric peaks, ECG peaks etc. It includes the complex and multiple peak detection algorithm. Has post-detection analyses including essential plots and statistical parameters. Group Analysis provides specialized and detailed analysis options for action potentials, decay fitting, fEPSP/population spikes, amperometry, etc.
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