Control of critical period development in mouse somatosensory cortex by glutamatergic signal transduction

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In the present study, I studied on the molecular mechanisms regulating critical period development of the mouse somatosensory cortex using gene knockout mice. In particular, I focused on the roles played by NMDA-type glutamate receptor subunits GluRe2 (NR2B) and GLuRe4 (NR2D) and also by glutamate transporter GLAST and GLT1 in developmental appearance, critical period termination, critical period plasticity of somatosensory barrel structures. Here I found that, compared to wild-type control mice, heterozygous GlnRe2+/-mice showed one-day retardation in developmental appearance and critical period termination, whereas homozygous GluRe4-/-mice did on-day facilitation. No significant change was seen in the magnitude of critical period plasticity, as determined by row-C whisker cautery. In contrast, homozygous GLAST-/-and GLTI-/-mice displayed significant reduction in the magnitude of critical period plasticity, with normal developmental appearance and critical period termination. These results provide experimental evidence that N3IDA receptor activation regulates temporal properties of somatosensory development in a subunit-dependent manner, while transporters regulating extracellular glutamate concentration magnify critical period plasticity. Therefore, armed with the two mechanisms, synaptic refinement during development is shaped normally in a activity-dependent manner.