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

Ciutat, Dolors; Calderó, Jordi; Oppenheim, Ronald W.; Esquerda, Josep E.

doi:10.1523/jneurosci.16-12-03979.1996

Cited by 72 publications

(54 citation statements)

References 49 publications

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“…Histopathological changes consisted of a severe interstitial edema, cellular swelling, and chromatin condensation that led to a massive and acute cytolysis, a dramatic neuronal depletion, and later gliosis; lumbar LMC MNs were almost completely depleted (Tables 1, 2). Ultrastructural morphology and in situ demonstration of DNA fragmentation of dying MNs indicated a necrotic, rather than apoptotic, mode of degeneration (Ciutat et al, 1996). Similar or even more extensive damage was obtained after treatment with either kainic acid or AMPA (0.1-0.5 mg) (Fig.…”

Section: Exposure To Excitatory Amino Acid Agonists Induces Acute Spisupporting

confidence: 63%

Opposing Effects of Excitatory Amino Acids on Chick Embryo Spinal Cord Motoneurons: Excitotoxic Degeneration or Prevention of Programmed Cell Death

et al. 1999

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Acute administration of a single dose of NMDA on embryonic day (E) 7 or later induces a marked excitotoxic injury in the chick spinal cord, including massive necrotic motoneuron (MN) death. When the same treatment was performed before E7, little, if any, excitotoxic response was observed. Chronic treatment with NMDA starting on E5 prevents the excitotoxic response produced by a later "acute" administration of NMDA. Additionally, chronic NMDA treatment also prevents the later excitotoxic injury induced by non-NMDA glutamate receptor agonists, such as kainate or AMPA. Chronic NMDA treatment also reduces normal MN death when treatment is maintained during the period of naturally occurring programmed cell death (PCD) of MNs and rescues MNs from PCD induced by early peripheral target deprivation. The trophic action of chronic NMDA treatment appears to involve a downregulation of glutamate receptors as shown by both a reduction in the obligatory NR1 subunit protein of the NMDA receptor and a decrease in the kainate-induced Co 2ϩ uptake in MNs. Both tolerance to excitotoxicity and trophic effects of chronic NMDA treatment are prevented by the NMDA receptor antagonist MK-801. Additionally, administration of MK-801 alone results in an increase in MN PCD. These data indicate for the first time that early activation of NMDA receptors in developing avian MNs in vivo has a trophic, survival-promoting effect, inhibiting PCD by a target-independent mechanism that involves NMDA receptor downregulation. Key words: excitatory amino acids; NMDA; motoneurons; programmed cell death; chick embryo; spinal cord; excitotoxicity; glutamate-induced neuroprotectionDuring the last two decades, programmed cell death (PCD) has been extensively recognized as a key feature of normal development of the nervous system. The pioneering studies of Viktor Hamburger and Rita Levi-Montalcini in the chick embryo have been substantiated by more recent studies showing that elimination of neuronal cells by PCD is essential for the correct assembly of the nervous system (for review, see Oppenheim, 1991). Lumbar spinal cord motoneurons (M Ns) in the chick embryo undergo PCD mainly in a well defined period extending from embryonic day (E) 6 to E12 (Hamburger, 1975;Chu-Wang and Oppenheim, 1978), leading to a 50% reduction of the initially differentiated MN pool. Neurotrophic factors and neuromuscular activity regulate the extent of the M N PCD (Pittman and Oppenheim, 1978;deLapeyrière and Henderson, 1997). E xcitatory amino acids, endogenously released by spinal cord interneurons, are involved in the generation of motor activity during development (Barry and O'Donovan, 1987). Although it is well established that glutamate receptors are important for synaptic differentiation and plasticity, the role of glutamate receptors in the regulation of normally occurring MN PCD has not been determined. In cultured neurons, glutamate may be either trophic or toxic for neurons according to the modulation of intracellular calcium levels (Choi, 1987;Balázs et al., 1988); mor...

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Section: Exposure To Excitatory Amino Acid Agonists Induces Acute Spisupporting

confidence: 63%

Opposing Effects of Excitatory Amino Acids on Chick Embryo Spinal Cord Motoneurons: Excitotoxic Degeneration or Prevention of Programmed Cell Death

et al. 1999

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“…Possibly axon retraction or degeneration, due to a lack of appropriate synapse formation, may have led to loss of some Schwann cells. Axon-derived trophic signals have been implicated in Schwann cell survival in avian peripheral nerves (Ciutat et al, 1996). Another possibility is that the method employed to detect Schwann cells (NGFr immunoreactivity) was not efficient for the longer survival times (see also Brook et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Spontaneous longitudinally orientated axonal regeneration is associated with the Schwann cell framework within the lesion site following spinal cord compression injury of the rat

et al. 1998

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Spontaneous cellular reorganisation at the lesion site has been investigated following massive spinal cord compression injury in adult rats. By 2 days post operation (p.o.), haemorrhagic necrosis, widespread axonal degeneration, and infiltration by polymorphnuclear granulocytes and OX42-positive macrophages were observed in the lesion site. By 7 days p.o., low affinity nerve growth factor receptor-positive Schwann cells, from activated spinal roots, were identified as they migrated far into the lesion. Between 7 and 14 days p.o., the overlapping processes of Schwann cells within the macrophage-filled lesion formed a glial framework which was associated with extensive longitudinally orientated ingrowth by many neurofilament-positive axons. Relatively few of these axons were calcitonin gene-related peptide (CGRP)-, substance P (SP)-, or serotonin (5HT)-positive; however, many were glycinergic or gamma aminobutyric acid (GABA)ergic. At 21 and 28 days p.o. (the longest survival times studied), a reduced but still substantial amount of orientated Schwann cells and axons could be detected at distances of up to 5 mm within the lesion. Glial fibrillary acidic protein (GFAP) immunoreactivity demonstrated the slow formation of astrocytic scarring which only became apparent at the lesion interface between 21 and 28 days p.o. The current data suggest the possibility of developing future therapeutic strategies designed to maintain or even enhance these spontaneous and orientated regenerative events.

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“…In both cases, the signal was identified as NRG1 (Dong et al, 1995(Dong et al, , 1999Jessen et al, 1994). Similarly, pharmacological and surgical-induced death of axons contributes to apoptotic Schwann cell death, and exogenous NRG1 administration can rescue death, induced by loss of axons (Ciutat et al, 1996;Winseck et al, 2002). Embryonic DRG axons and motor neurons express NRG1, which accumulates along axonal tracts (Falls et al, 1993;Loeb et al, 1999;Marchionni et al, 1993;Orr-Urtreger et al, 1993, Taveggia et al, 2005 and would therefore be available at the right time to regulate precursor survival.…”

Section: Axonal-glial Interactions In Developing Nerves and Their Impmentioning

confidence: 99%

Development of the Schwann cell lineage: From the neural crest to the myelinated nerve

Woodhoo

Sommer

2008

Glia

203

185

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The myelinating and nonmyelinating Schwann cells in peripheral nerves are derived from the neural crest, which is a transient and multipotent embryonic structure that also generates the other main glial subtypes of the peripheral nervous system (PNS). Schwann cell development occurs through a series of transitional embryonic and postnatal phases, which are tightly regulated by a number of signals. During the early embryonic phases, neural crest cells are specified to give rise to Schwann cell precursors, which represent the first transitional stage in the Schwann cell lineage, and these then generate the immature Schwann cells. At birth, the immature Schwann cells differentiate into either the myelinating or nonmyelinating Schwann cells that populate the mature nerve trunks. In this review, we will discuss the biology of the transitional stages in embryonic and early postnatal Schwann cell development, including the phenotypic differences between them and the recently identified signaling pathways, which control their differentiation and maintenance. In addition, the role and importance of the microenvironment in which glial differentiation takes place will be discussed. V V C 2008 Wiley-Liss, Inc.

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

Cited by 72 publications

References 49 publications

Opposing Effects of Excitatory Amino Acids on Chick Embryo Spinal Cord Motoneurons: Excitotoxic Degeneration or Prevention of Programmed Cell Death

Opposing Effects of Excitatory Amino Acids on Chick Embryo Spinal Cord Motoneurons: Excitotoxic Degeneration or Prevention of Programmed Cell Death

Spontaneous longitudinally orientated axonal regeneration is associated with the Schwann cell framework within the lesion site following spinal cord compression injury of the rat

Development of the Schwann cell lineage: From the neural crest to the myelinated nerve

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