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Neural Plasticity
Volume 2012 (2012), Article ID 797295, 10 pages
Review Article

Activity-Dependent Callosal Axon Projections in Neonatal Mouse Cerebral Cortex

1Department of Biophysics, Kyoto University Graduate School of Science, Kitashirakawa-Oiwake-cho, Sakyo-ku, Kyoto 606-8502, Japan
2CREST, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan

Received 31 July 2012; Accepted 21 October 2012

Academic Editor: Matteo Caleo

Copyright © 2012 Yoshiaki Tagawa and Tomoo Hirano. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Callosal axon projections are among the major long-range axonal projections in the mammalian brain. They are formed during the prenatal and early postnatal periods in the mouse, and their development relies on both activity-independent and -dependent mechanisms. In this paper, we review recent findings about the roles of neuronal activity in callosal axon projections. In addition to the well-documented role of sensory-driven neuronal activity, recent studies using in utero electroporation demonstrated an essential role of spontaneous neuronal activity generated in neonatal cortical circuits. Both presynaptic and postsynaptic neuronal activities are critically involved in the axon development. Studies have begun to reveal intracellular signaling pathway which works downstream of neuronal activity. We also review several distinct patterns of neuronal activity observed in the developing cerebral cortex, which might play roles in activity-dependent circuit construction. Such neuronal activity during the neonatal period can be disrupted by genetic factors, such as mutations in ion channels. It has been speculated that abnormal activity caused by such factors may affect activity-dependent circuit construction, leading to some developmental disorders. We discuss a possibility that genetic mutation in ion channels may impair callosal axon projections through an activity-dependent mechanism.