Preferential loss of collaterals from goldfish retinal axons in the optic tract is delayed by tetrodotoxin.
Following optic nerve section (ONS) in goldfish, the right eye was repeatedly injected with tetrodotoxin (TTX) and the left eye with Ringer solution. At various survival periods after ONS, horseradish peroxidase (HRP) was applied to small groups of axons in dorsal or ventral retina in both eyes. Counts of labeled regenerating retinal axons show that 43 +/- 4.6% of regenerating axons course through the inappropriate brachium of the optic tract between 20 and 65 days after ONS. The amount of misrouted axons declines to 30 +/- 6.1% between 70 and 80 days after ONS. Under TTX blockade the reduction of misrouted axons is delayed but reaches 27 +/- 3.6% at 150 days after ONS.
Hartlieb
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E
Friedrich-Miescher-Laboratorium der Max-Planck-Gesellschaft, Tübingen, F.R.G.
Stuermer
C A
CA
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology*; D002452:Cell Count; D003530:Cyprinidae / Q000502:physiology*; D006054:Goldfish / Q000502:physiology*; D009416:Nerve Regeneration / Q000187:drug effects*; D009900:Optic Nerve / Q000166:cytology / Q000502:physiology*; D012160:Retina / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D013779:Tetrodotoxin / Q000494:pharmacology*; D013997:Time Factors
D013779:Tetrodotoxin