Timing of neuronal death following successive blockade of protein synthesis and axoplasmic transport in the axonal target territory.
Neurons in the isthmo-optic nucleus (ION) of chick embryos can withstand a substantial cycloheximide-induced reduction in protein synthesis in their target territory, the retina, at the very time when their survival is known to depend on a retrograde signal from the latter. We here test the hypothesis that this resistance to the cycloheximide injection might be due to the accumulation in the ION of a reserve of retina-derived trophic molecules (or of resulting second messengers). Following an intraocular injection of cycloheximide at E15 to deplete the hypothetical reserve in one ION, both eyes received injections of colchicine (which blocks axoplasmic transport) at E16. The resulting time course of cell death was very similar in the two IONs, which refutes the hypothesis. The most plausible alternative is that there is a reserve of trophic substance in the retina capable of maintaining the ION for about 1 day.
Blaser
P F
PF
Institute of Anatomy, University of Lausanne, Switzerland.
Clarke
P G
PG
D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D001369:Axons / Q000187:drug effects*; D016923:Cell Death / Q000187:drug effects; D002642:Chick Embryo; D003078:Colchicine / Q000494:pharmacology; D003513:Cycloheximide / Q000008:administration & dosage / Q000494:pharmacology; D005123:Eye / Q000196:embryology; D007267:Injections; D009474:Neurons / Q000187:drug effects*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology*; D012160:Retina / Q000166:cytology / Q000196:embryology
D011500:Protein Synthesis Inhibitors; D003513:Cycloheximide; D003078:Colchicine