Table 1.

Pathfinding defects observed in oligonucleotide-injected brains

No obvious pathfinding defects Subtle pathfinding defect Mild pathfinding defect Severe pathfinding defect
Precrossing axons
E15 antisense 1 1 2 2
E15 control 6 0 0 0
E16 antisensea 3 2 8 9
E16 control 19 0 0 0
Postcrossing axons
E16 antisensea 2 2 4 1
E16 control 8 0 0 0
  • Precrossing axons were defined as axons labeled with a carbocyanine dye injection in the same hemisphere as the oliognucleotide injection. These were pooled from brains labeled in with a dye injection in only one hemisphere and brains labeled with a dye injection in both hemispheres. Postcrossing axons were analyzed from brains injected with a dye in both hemispheres. Pathfinding defects were defined as “subtle” if the axons were only defasiculated, “mild” in cases in which the axons were both defasiculated and a few axons grew aberrantly into the septum or the glial wedge, and “severe” in cases in which the axons were defasiculated and most grew into the septum or the glial wedge or formed Probst-like bundles.

  • a Note that in the two cases of antisense oligonucleotide-injected brains in which postcrossing axons displayed no obvious pathfinding defects, the precrossing axons in the same brain were also unaffected and make up two-thirds of the brains indicated as having no obvious pathfinding defects in the precrossing total. In these cases, it is, therefore, possible that the antisense oliognucleotide injections were not effective in reducing the levels of Slit2 protein.