In the nervous system of vertebrates, myelination is essential for rapid and accurate impulse conduction. Myelin thickness depends on axon fiber size. We use mutant and transgenic mouse lines to show that axonal Neuregulin-1 (Nrg1) signals information about axon size to Schwann cells. Reduced Nrg1 expression causes hypomyelination and reduced nerve conduction velocity. Neuronal overexpression of Nrg1 induces hypermyelination and demonstrates that Nrg1 type III is the responsible isoform. We suggest a model by which myelin-forming Schwann cells integrate axonal Nrg1 signals as a biochemical measure of axon size.

Luminance contrast sensitivity and colour contrast thresholds were determined in 26 Parkinson patients and 17 normal controls of comparable age. They were psychophysically tested with a colour monitor system. Stimuli consisted of Gaussian enveloped luminance modulated or colour modulated (protan and tritan axis) vertical sine wave gratings with a spatial frequency of 1 cycle/degree. The stimuli subtended 4 degrees in diameter. Thresholds were determined using a two alternative forced choice method. Three different experimental conditions were explored: the detectability of stationary gratings, of moving gratings at velocities of 0, 2.5 and 5.0 cycles/s, and the detectability of horizontal square wave displacement at a frequency of 5 Hz for gratings of specified contrast levels. Intergroup differences were evaluated using two-tailed t tests with Satterthwaite corrections. Consistent and significant differences between normals and patients were found for tritan stimuli in the static and both dynamic conditions, and for luminance contrast stimuli in the displacement condition. Protan stimuli were much less apt to detect differences between the groups. We conclude that the retinal deficit of dopamine in Parkinson's disease is reflected in diminished centre/surround inhibition and that these changes are primarily apparent when vision is tested along the tritan axis, because blue cones are sparsely distributed.