Rapid appearance of labeled degenerating cells in the dorsal root ganglia after exposure of chick embryos to tritiated thymidine

Carr, Virginia McMillan; Simpson, Sidney B.

doi:10.1016/0165-3806(81)90066-3

Cited by 41 publications

(11 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have shown that dying cells are involved in DNA synthesis shortly before death (Carr and Simpson, 1981;Homma et al, 1994;Blaschke et al, 1996Blaschke et al, , 1998Galli-Resta and Ensini, 1996;Thomaidou et al, 1997;Diaz et al, 1999;Lossi and Merighi, 2003) or express markers of proliferating cells, such as Ki67, or neural stem cells, such as nestin (Depaepe et al, 2005). Consequently, decreased cell death in the ventricular layer, where actively dividing neuroepithelial progenitors are located, has been found in the knockout mice for caspase-3, caspase-9, Apaf-1, and Cyt c KA/KA .…”

Section: Early Neural Cell Death Is Associated With Multiple Cellularmentioning

confidence: 94%

Cell death in early neural life

Boya

Rosa

2005

Birth Defect Res C

View full text Add to dashboard Cite

Programmed cell death is a relevant process in the physiology and pathology of the nervous system. Neuronal cell death during development is well characterized, and studies of this process have provided valuable information regarding the regulatory mechanisms of cell death in the nervous system. In the last few years, cell death occurring at earlier developmental stages and affecting proliferating neuroepithelial cells and recently born neuroblasts has been recognized. In this review we cover the observations on cell death in the early, proliferating stages of vertebrate neural development. Genetically modified mouse model systems and complementary in vivo approaches in other vertebrates have provided a solid basis for its relevance and contribution to normal neural development, as well as for the pathological consequences of its deregulation. However, the precise functional role of cell death remains a topic of debate.

show abstract

Section: Early Neural Cell Death Is Associated With Multiple Cellularmentioning

confidence: 94%

Cell death in early neural life

Boya

Rosa

2005

Birth Defect Res C

View full text Add to dashboard Cite

show abstract

“…Although dying embryonic cells have been reported in proliferative zones during neurogenesis (see, e.g., Carr and Simpson, 1981;Homma et al, 1994;Blaschke et al, 1996), the term NND is usually restricted to a later ontogenic period when a significant fraction of differentiating neurons die while forming functional connections with their target field (for reviews, see Cowan et al, 1984;Oppenheim, 1991;Clarke, 1994). NND is thought to assist in the development of functional connectivity by eliminating erroneously projecting neurons and by matching numbers of neurons between projection and target nuclei (Cowan et al, 1984).…”

mentioning

confidence: 99%

Naturally occurring neuron death during postnatal development of the gerbil ventral cochlear nucleus begins at the onset of hearing

Tierney

Moore

1997

J. Comp. Neurol.

View full text Add to dashboard Cite

Postnatal development of the gerbil ventral cochlear nucleus (VCN) was studied quantitatively under the light microscope in Nissl-stained serial sections at postnatal day 0 (P0), P5, P7, P10, P12, P15, and P140. VCN boundaries were unambiguous at all ages, and nucleus volume was calculated planimetrically for all groups. Measurements of neuron soma cross-sectional area and number were made in all groups except P0. Both VCN volume and soma area doubled between P5 and P10. Although somatic growth did not continue beyond P10, VCN volume increased a further 57% between P15 and P140. Neuron number did not change significantly between P5 and P10, averaging approximately 36,000 neurons. Between P10 and P12, neuron number decreased significantly by 22%, with no further change thereafter. Our data show that, following significant postnatal growth in the gerbil VCN, a brief period of naturally occurring neuron death begins at the onset of hearing.

show abstract

“…Their interpretation was that the accelerated cell death represented a modification of the normal mechanisms, where death is thought to result from the competition for trophic macromolecules supplied by the periphery. Work by Carr and Simpson (1982) in the DRG indicates that the interactions between embryonic sensory neurons and the periphery are more complicated than previously proposed, and they suggest a role for local as well as distant trophic factors in mediating neuron survival. The question of whether the accelerated death of motoneurons in the absence of the developing limb bud is the same as normal motoneuron death remains open.…”

Section: Discussionmentioning

confidence: 77%

Survival of motoneurons in the brachial lateral motor column of limbless mutant chick embryos depends on the periphery

Jl¹,

Fallon²

1986

J. Neurosci.

View full text Add to dashboard Cite

Motoneuron survival in the embryonic spinal cord is influenced by the presence or absence of the developing limb bud. We have recently begun a reexamination of the relationship between limb absence and motoneuron survival in a nonsurgical limb deletion model, the limbless mutant chick embryo. As in surgically limbdeleted normal embryos, only 10% of the motoneurons that are intially produced in the limbless mutant lateral motor column (LMC) survive the embryonic period (Lanser and Fallon, 1984). We now report' that, when supplied with a normal periphery (i.e., a normal limb bud), more than 40% of the motoneurons initially produced in the limbless LMC survive the embryonic period. Motoneuron cell counts in one-winged limbless embryos reveal that over 3.5 times as many motoneurons survive the cell death period in the LMC on the side with the limb than on the opposite, limbless side. This demonstrates the dependence of embryonic LMC motoneurons on the developing limb for survival and indicates that the limbless mutant is an appropriate model for studying the death and survival of LMC motoneurons during development. Using the limbless mutant to study LMC motoneuron survival eliminates the complication of possible direct surgical effects on motoneuron death. In addition, we found that a substantial effect of the wing on rescuing LMC motoneurons was exerted prior to the 6th day of embryonic development. Normally, little cell loss occurs in the brachial LMC during this time. Accordingly, motoneuron death in the limb-deprived brachial LMC, whether in surgically limb-deleted normal embryos or in genetically limbless embryos, is accelerated with respect to cell death in the normal brachial LMC.Since cell death was first established as an integral part of the development of specific nerve centers (Hamburger and LeviMontalcini, 1949), the phenomenon of naturally occurring neuronal death has been widely documented but incompletely understood (for a historical review, see Oppenheim, 198 1). One neuronal population where cell death has been extensively studied is the lateral motor column (LMC) of the spinal cord (see Lamb, 1984, for review). The LMC contains the motoneurons that innervate the muscles of the vertebrate limb. It has been

show abstract

Rapid appearance of labeled degenerating cells in the dorsal root ganglia after exposure of chick embryos to tritiated thymidine

Cited by 41 publications

References 7 publications

Cell death in early neural life

Cell death in early neural life

Naturally occurring neuron death during postnatal development of the gerbil ventral cochlear nucleus begins at the onset of hearing

Survival of motoneurons in the brachial lateral motor column of limbless mutant chick embryos depends on the periphery

Contact Info

Product

Resources

About