Plasticity of Neuronal Circuits in the Mammalian Brain
Nobuhiko Yamamoto
Laboratory of Cellular and Molecular Neurobiology, Osaka University
The most interesting aspect in neuronal wiring is plasticity. We previously demonstrated that neuronal activity increases thalamocortical axon branching in sensory cortex. Our investigation of the molecular mechanism further suggests that Netrin-4 and Bdnf contribute to activity-dependent branch formation. The next intriguing question is how neuronal activity is converted into the molecular signals. To address this issue, we have been investigating dynamics of activity-dependent transcription factors by a single molecule imaging technique. The result demonstrated that repetitive binding of CREB to specific genome locations takes place by increasing neuronal activity. On the other hand, neuronal connections are also known to remodel after the brain injury, which is also due to a plastic property of the nervous system. A good example is that contralateral corticomecencephalic projection emerges after unilateral cortical ablation. Our recent study indicates that after hemispherectomy glial cell-derived factors are expressed in the denervated mid brain and promote the ectopic contralateral projection. Here I will discuss the plasticity of neuronal circuit formation by introducing the above two distinct topics.
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