Linked Life Data

9412513

Source:http://linkedlifedata.com/resource/pubmed/id/9412513

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-1-16
pubmed:abstractText
Unilateral limb-bud removal (LBR) before the outgrowth of sensory or motor neurons to the leg of chick embryos was used to examine the role of limb (target)-derived signals in the development and survival of lumbar motoneurons and sensory neurons in the dorsal root ganglia (DRG). After LBR, motor and sensory neurons underwent normal initial histological differentiation, and cell growth in both populations was unaffected. Before their death, target-deprived motoneurons also expressed a cell-specific marker, the homeodomain protein islet-1. Proliferation of sensory and motor precursor cells was also unaffected by LBR, and the migration of neural crest cells to the DRG and of motoneurons into the ventral horn occurred normally. During the normal period of programmed cell death (PCD), increased numbers of both sensory and motor neurons degenerated after LBR. However, whereas motoneuron loss increased by 40-50% (90% total), only approximately 25% more sensory neurons degenerated after LBR. A significant number of the surviving sensory neurons projected to aberrant targets in the tail after LBR, and many of these were lost after ablation of both the limb and tail. Treatment with neurotrophic factors (or muscle extract) rescued sensory and motor neurons from cell death after LBR without affecting precursor proliferation of either population. Activity blockade with curare failed to rescue motoneurons after LBR, and combined treatment with curare plus muscle extract was no more effective than muscle extract alone. Treatment with the antioxidant N-acetylcysteine rescued motoneurons from normal cell death but not after LBR. Two specific inhibitors of the interleukin beta1 converting enzyme (ICE) family of cysteine proteases also failed to prevent motoneuron death after LBR. Taken together these data provide definitive evidence that the loss of spinal neurons after LBR cannot be attributed to altered proliferation, migration, or differentiation. Rather, in the absence of limb-derived trophic signals, the affected neurons fail to survive and undergo PCD. Although normal cell death and cell death after target deprivation share many features in common, the intracellular pathways of cell death in the two may be distinct.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
356-70
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9412513-Acetylcysteine, pubmed-meshheading:9412513-Amino Acid Chloromethyl Ketones, pubmed-meshheading:9412513-Animals, pubmed-meshheading:9412513-Axons, pubmed-meshheading:9412513-Brain-Derived Neurotrophic Factor, pubmed-meshheading:9412513-Cell Count, pubmed-meshheading:9412513-Cell Death, pubmed-meshheading:9412513-Cell Differentiation, pubmed-meshheading:9412513-Cell Survival, pubmed-meshheading:9412513-Chick Embryo, pubmed-meshheading:9412513-Cysteine Proteinase Inhibitors, pubmed-meshheading:9412513-Free Radical Scavengers, pubmed-meshheading:9412513-Ganglia, Spinal, pubmed-meshheading:9412513-Limb Buds, pubmed-meshheading:9412513-Motor Neurons, pubmed-meshheading:9412513-Nerve Growth Factors, pubmed-meshheading:9412513-Neurons, Afferent, pubmed-meshheading:9412513-Neurotrophin 3, pubmed-meshheading:9412513-Oligopeptides, pubmed-meshheading:9412513-Spinal Cord
pubmed:year
1998
pubmed:articleTitle
Peripheral target regulation of the development and survival of spinal sensory and motor neurons in the chick embryo.
pubmed:affiliation
Department of Basic Medical Sciences, University of Lleida, Lleida 25198, Catalonia, Spain.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't