Figure 9.

Absence of schizophrenia-like abnormalities in adult mice acutely treated with anti-Nogo-A antibodies for 2 weeks. A–C, Comparative regional antibody distribution in cervical spinal cord after intrathecal lumbar delivery of anti-Nogo-A or control IgG antibody via osmotic minipumps. Color coding of sections processed for immunoperoxidase staining ranges from black/dark blue, for background, to violet, red, orange, yellow, and white, for maximal staining intensity. Note the clear difference in antibody levels between the treatment groups. D, Representative image of antibody detection in the cortex of an anti-Nogo-A antibody-treated animal. Stained cell bodies reflect uptake of Nogo-A–anti-Nogo-A antibody complexes as shown earlier (Weinmann et al., 2006). E, Sensitivity of mice to the motor stimulant effects of systemic amphetamine. Locomotor activating effect of amphetamine is expressed as overall mean distance traveled during the 120 min observation period. Anti-Nogo-A antibody treatment did not significantly affect the locomotor reactivity to the drug (n = 9/group). F, G, Representative images of D2R immunostaining in the dorsal striatum of mice treated with either anti-Nogo-A or control antibodies. H, Quantitative analysis of the D2R staining. The relative optical density of D2R in the medial prefrontal cortex (mPFC), the dorsal striatum (CPu), and the nucleus accumbens core (NAcC) and shell (NAcS) regions, was not affected by the anti-Nogo-A antibody treatment (n = 5/group). All values are mean ± SEM. Scale bars: A–C, 0.5 mm; D, 20 μm; F, G, 100 μm. 11C7, Anti-Nogo-A antibody treated; IgG, control IgG treated; no pump, no pump control.