Figure 1.

BDNF-dependent reversal of MAG-mediated inhibition is sAC dependent, but not tmAC dependent. Rat P5–P6 CGNs were isolated and treated with pharmacological tmAC inhibitor, ddAdo (A, B), or sAC-specific pharmacological inhibitors, KH7 (C, D) and OH-E (E, F) ± BDNF for 15–17 h, before being transferred onto monolayers of either MAG-expressing CHO cells or control CHO cells for 22 h (A, C, E) or onto purified myelin or PLL control for 26 h (B, D, F). Neurons were fixed and stained for β-III-tubulin. Results represent the percentage of the average length of the longest neurite over the control from 500 to 800 neurons ± SEM; n = 3–4, *p < 0.05, **p < 0.01, ***p < 0.001.