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The Journal of Neuroscience, 1999, 19:RC40:1-5

RAPID COMMUNICATION
Brain-derived Neurotrophic Factor Overexpression Induces Precocious Critical Period in Mouse Visual Cortex

Jessica L. Hanover¹, Z. Josh Huang², Susumu Tonegawa^{2, 3}, and Michael P. Stryker¹

¹ Neuroscience Graduate Program and Department of Physiology, University of California, San Francisco, California, 94143, and ² Howard Hughes Medical Institute, Center for Learning and Memory, Center for Cancer Research and Department of Biology, and ³ Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139

Brain-derived neurotrophic factor (BDNF) is a candidate molecule for regulating activity-dependent synaptic plasticity on the grounds of its expression pattern in developing visual cortex and that of its receptor, trkB (Castrén et al., 1992; Bozzi et al., 1995; Schoups et al., 1995; Cabelli et al., 1996), as well as the modulation of these patterns by activity (Castrén et al., 1992; Bozzi et al., 1995; Schoups et al., 1995). Infusing trkB ligands or their neutralizing agents, the trkB-IgG fusion proteins, into visual cortex alters the development and plasticity of ocular dominance columns (Cabelli et al., 1995; Riddle et al., 1995; Galuske et al., 1996; Gillespie et al., 1996; Cabelli et al., 1997). To test further the physiological role of BDNF, we studied a transgenic mouse that expresses elevated levels of BDNF in primary visual cortex (V1) postnatally (Huang et al., 1999). We found that unlike the infusion experiments, excess BDNF expressed in mouse visual cortex did not block ocular dominance plasticity. Instead, single neurons in V1 of the BDNF transgenic mice were as susceptible to the effects of monocular deprivation (MD) as neurons in wild-type mice, but only during a precocious critical period. At a time when V1 in the wild-type mouse responded maximally to a 4 d MD with a reduction in its response to deprived eye visual stimulation, the transgenic mouse V1 had already passed the peak of its precocious critical period and no longer responded maximally. This finding suggests a role for BDNF in promoting the postnatal maturation of cortical circuitry.

Key words: BDNF; visual cortex; critical period; neurotrophin; trkB; ocular dominance; plasticity; transgenic mouse

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Copyright © 0000 Society for Neuroscience  0270-6474/0/$05.00/0

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