Axonal regeneration was inhibited by morpholino antisense oligonucleotides for NF180.

<p><b>A,</b> Spinal-projecting axons were retrogradely labeled with a DTMR-conjugated control MO or a fluorescein-conjugated NF180 antisense MO. At 2 weeks post-TX, axon tips had retracted slightly farther in the control group than in the antisense group (not statistically significant). At 4 weeks, spinal-projecting axons in the control group had regenerated significantly closer to the transection site than had the antisense group (p<0.01); n = the number of axons measured. The number of animals used for each experiment is given in <a href="" target="_blank">Table 1</a>. Because optical isolation of individual axon tips can be difficult in these whole, living spinal cords, each animal provided only a few axons for which tip positions could be measured. Thus within treatment groups, it was more meaningful to pool axons from multiple animals in order to calculate mean axon regeneration rates, than to calculate mean regeneration rates for each animal and then compare those means. <b>B,</b> Decrease in the fraction of MO-labeled neurons whose axon had regenerated beyond the site of a second retrograde label applied 5 mm caudal to original TX at 9 weeks post-TX, and were therefore double-labeled. * indicates difference from control is significant at p<0.001 (student’s <i>t</i> test).</p>