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First published online 23 March 2005
doi: 10.1242/dev.01798
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1 Departments of Anesthesiology, Psychiatry, Molecular Biology and Pharmacology,
School of Medicine, Washington University Pain Center, St Louis, MO 63110,
USA
2 Anatomy and Neurobiology, School of Medicine, Washington University Pain
Center, St Louis, MO 63110, USA
Author for correspondence (e-mail:
chenz{at}wustl.edu)
Accepted 15 February 2005
Neuronal migration and lamina-specific primary afferent projections are crucial for establishing spinal cord circuits, but the underlying mechanisms are poorly understood. Here, we report that in mice lacking Dcc (deleted in colorectal cancer), some early-born neurons could not migrate ventrally in the spinal cord. Conversely, forced expression of Dcc caused ventral migration and prevented dorsolateral migration of late-born spinal neurons. In the superficial layer of the spinal cord of Dcc/ mutants, mislocalized neurons are followed by proprioceptive afferents, while their presence repels nociceptive afferents through Sema3a. Thus, our study has shown that Dcc is a key molecule required for ventral migration of early-born neurons, and that appropriate neuronal migration is a prerequisite for, and coupled to, normal projections of primary afferents in the developing spinal cord.
Key words: Dcc, Early-born neuron, Migration, Primary afferents, Spinal cord, Mouse
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