as failure of axons to cross the midline have been attributed to DCC signaling insufficiency, even when loss of Dcc expression and function are only partial [21, 24, 39]. The Dcc gene itself codes for a single transmembrane spanning receptor protein. It controls the guidance of axons (and dendrites) towards sources of netrin-1, but it is also involved in additional events including axon differentiation and synaptogenesis [21, 27, 35, 37]. Our observations of spinal cord nociceptive fiber innervation suggest that certain basic nociceptive connections may be intact in dcc heterozygous mice, but we cannot rule out functionally important spinal cord structural differences that would require more detailed study to detect.
