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Volume 16, Number 12, Issue of June 15, 1996 pp. 3979-3990
Copyright ©1996 Society for Neuroscience

Schwann Cell Apoptosis during Normal Development and after Axonal Degeneration Induced by Neurotoxins in the Chick Embryo

Received Jan. 29, 1996; revised March 26, 1996; accepted March 29, 1996.

Dolors Ciutat¹, Jordi Calderó¹, Ronald W. Oppenheim², and Josep E. Esquerda¹

¹ Unitat de Neurobiologia Cel.lular, Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida, 25198 Lleida, Catalonia, Spain, and ² Department of Neurobiology and Anatomy and Neuroscience Program, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157

In the present work, we show that chick embryo Schwann cells die by apoptosis both during normal development and after axonal degeneration induced by neurotoxin treatment. Schwann cell apoptosis during development takes place during a period roughly coincidental with normally occurring motoneuron death. Administration of NMDA to chick embryos on embryonic day 7 induces extensive excitotoxic motoneuronal damage in the spinal cord without any apparent effects on neurons in the dorsal root ganglia (DRG). The death of Schwann cells in ventral nerve roots after NMDA treatment causes degenerative changes that display ultrastructural features of apoptosis and exhibit in situ detectable DNA fragmentation. By contrast, NMDA treatment does not increase the death of Schwann cells in dorsal nerve roots. In situ detection of DNA fragmentation in combination with the avian Schwann cell marker 1E8 antibody demonstrates that dying cells in ventral nerve roots are in the Schwann cell lineage. Administration of cycloheximide does not prevent the toxic effects of NMDA on motoneurons, but dramatically reduces the number of pyknotic Schwann cells and DNA fragmentation profiles in the ventral nerve roots. In ovo administration of various tissue extracts (muscle, brain, and spinal cord) from the chick embryo or of the motoneuron conditioned medium fails to prevent Schwann cell apoptosis in NMDA-treated embryos. Intramuscular administration of the snake toxin -bungarotoxin produces a massive death of both lateral motor column motoneurons and DRG neurons, resulting in a substantial increase in the number of pyknotic Schwann cells in both ventral and dorsal nerve roots. It is concluded that during development, axonal-derived trophic signals are involved in the regulation of Schwann cell survival in peripheral nerves.

Key words: Schwann cells; apoptosis; peripheral nerves; development; excitotoxicity; -bungarotoxin; chick embryo

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