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Fig. 4. Axon guidance defects caused by application of metalloproteinase inhibitors
as RGC axons cross the optic chiasm. Vibratome (50 µm) sections through the
diencephalon and eyes of embryos exposed at stage 31 to either control (A,C),
SB-3CT (B,D,E) or GM6001 (H,I) solutions. The HRP-labelled optic projections
are visible. (A,C) In control, RGC axons cross the midline at the optic chiasm
and grow dorsally through the diencephalon to innervate the optic tectum. C is
a higher power view of the optic chiasm shown in A. (B,D,E) In the 25 µM
SB-3CT-treated brains, RGC axons often failed to enter the contralateral
diencephalon (star), or grew aberrantly into the contralateral optic nerve
(arrows). E is a higher power view of the optic projection shown in B and D is
another example of a 25 µM SB-3CT-treated brain. (F,G) Fluorescent
micrographs of the HRP-labelled optic projections in 12 µm transverse
cryostat sections through the optic chiasm in the ventral diencephalon.
Control axons shown in F cross the midline (arrow), whereas SB-3CT treated
axons (G) stalled at the midline (arrow). (G) A more weakly labelled optic
projection was chosen for visualization purposes. (H,I) Similar axonal
phenotypes are observed in a 10 µM GM6001-treated brain. (H) Axons in the
optic chiasm are seen to defasciculate (arrowheads). In a more caudal section
(I), axons are seen within the contralateral eye (arrowhead). Tec, tectum; D,
dorsal; V, ventral; oc, optic chiasm; R, retina. Scale bar: 50 µm for
A,B,H,I; 25 µm for C-G.
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