INFLUENCE OF MITOCHONDRIAL PROTEIN-SYNTHESIS INHIBITION ON DEAFFERENTATION-INDUCED ULTRASTRUCTURAL-CHANGES IN NUCLEUS MAGNOCELLULARIS OF DEVELOPING CHICKS

Following cochlea removal in developing chicks, about 30% of the neuro ns in the ipsilateral second-order auditory nucleus, nucleus magnocell ularis, undergo cell death. Administration of chloramphenicol, a mitoc hondrial protein synthesis inhibitor, results in a pronounced increase in deafferentation-induced cell death. In this study, we examined whe ther the chloramphenicol enhancement of deafferentation-induced cell d eath reveals the same ultrastructural characteristics that are seen in degenerating nucleus magnocellularis neurons after cochlea removal al one. Unilateral cochlea removal was performed on anaesthetized posthat ch chicks. One group of animals was simultaneously treated with chlora mphenicol. Six, twelve, or twenty-four hours following cochlea removal , n. magnocellularis neurons were studied by routine transmission elec tron microscopy. Particular attention was paid to the integrity of the polyribosomes and rough endoplasmic reticulum. Two ultrastructurally different types of neuronal degeneration were observed in the deaffere nted nucleus magnocellularis neurons: an early onset electron-lucent t ype that always involved ribosomal dissociation and a late-onset elect ron-dense type displaying nuclear pyknosis and severely damaged mitoch ondria, The percentage of nucleus magnocellularis neurons displaying r ibosomal disintegration following cochlea removal was found to be mark edly increased after chloramphenicol treatment. This finding suggests that mitochondrial function is important for the maintenance of a func tional protein synthesis apparatus following deafferentation. (C) 1996 Wiley-Liss, Inc