Neuromuscular blockade increases motoneurone survival during normal cell death in the chick embryo

Nature ◽  
1978 ◽  
Vol 271 (5643) ◽  
pp. 364-366 ◽  
Author(s):  
R. H. PITTMAN ◽  
R. W. OPPENHEIM
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Neuromuscular Blockade ◽  
Normal Cell

Cell death of motoneurons in the chick embryo spinal cord. XI. Acetylcholine receptors and synaptogenesis in skeletal muscle following the reduction of motoneuron death by neuromuscular blockade

Development ◽  
1989 ◽  
Vol 107 (2) ◽  
pp. 331-341
Author(s):  
R.W. Oppenheim ◽  
S. Bursztajn ◽  
D. Prevette
Keyword(s):  
Skeletal Muscle ◽  
Cell Death ◽  
Neuromuscular Blockade ◽  
Normal Cell ◽  
Cell Loss ◽  
Complete Recovery ◽  
Neuromuscular Blocking ◽  
Motoneuron Survival ◽  
Neuromuscular Activity ◽  
Induced Changes

Treatment of chick embryos with neuromuscular blocking agents such as curare during periods of naturally occurring motoneuron death results in a striking reduction of this normal cell loss. Inactivity-induced changes in motoneuron survival were found to be associated with increased levels of AChRs and AChR-clusters in skeletal muscle and with increased focal sites of AChE that are innervated (‘synaptic sites’). Treatment of embryos with curare after the normal cell death period (E12-E15) resulted in no change in motoneuron survival. Although AChR-clusters and focal sites of AChE were increased in these embryos on E16, many of these sites were uninnervated. Treatment of embryos with nicotine or decamethonium (E6-E10) also reduced neuromuscular activity but did not alter motoneuron survival nor did such treatment alter AChRs. The different effects of curare vs nicotine and decamethoniam on motoneuron survival and AChRs may be related to the fact that the former is a competitive blocker whereas the latter two drugs are depolarizing blockers. Finally, treatment of embryos (E6-9) with doses of curare (1 mg daily) that allow for the almost complete recovery of neuromuscular activity a few days following treatment (by E16) resulted in the gradual loss of the excess motoneurons that were present on E10, and by E16 the number of remaining AChR clusters and focal sites of AChE were also decreased to levels comparable to control values. Inactivity-induced changes in AChRs or AChR-clusters may be an important factor in the reduced motoneuron death that accompanies neuromuscular blockade during critical stages of development. These receptor changes very likely reflect increased synaptogenesis in the muscles of paralyzed embryos which in turn may act to reduce motoneuron death by providing increased access to muscle-derived neurotrophic molecules.

vitreal cells and specialized phagocytes in the chick embryo retina: A TEM and SEM study

1990 ◽  
Vol 48 (3) ◽  
pp. 330-331
Author(s):  
M.A. Cuadros ◽  
M.J. Martinez-Guerrero ◽  
A. Rios
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Acid Phosphatase ◽  
Chick Embryo ◽  
Basement Membrane ◽  
Sem Images ◽  
Intimate Contact ◽  
Cellular Processes ◽  
Sem Study ◽  
Free Cells

In the chick embryo retina (days 3-4 of incubation), coinciding with an increase in cell death, specialized phagocytes characterized by intense acid phosphatase activity have been described. In these preparations, all free cells in the vitreal humor (vitreal cells) were strongly labeled. Conventional TEM and SEM techniques were used to characterize them and attempt to determine their relationship with retinal phagocytes.Two types of vitreal cells were distinguished. The first are located at some distance from the basement membrane of the neuroepithelium, and are rounded, with numerous vacuoles and thin cytoplasmic prolongations. Images of exo- and or endocytosis were frequent; the cells showed a well-developed Golgi apparatus (Fig. 1) In SEM images, the cells was covered with short cellular processes (Fig. 3). Cells lying parallel to or alongside the basement membrane are elongated. The plasma membrane is frequently in intimate contact with the basement membrane. These cells have generally a large cytoplasmic expansion (Fig. 5).

Truncated wild-type SOD1 and FALS-linked mutant SOD1 cause neural cell death in the chick embryo spinal cord

2006 ◽  
Vol 21 (1) ◽  
pp. 194-205 ◽  
Author(s):  
Ghanashyam D. Ghadge ◽  
Lijun Wang ◽  
Kamal Sharma ◽  
Anna Liza Monti ◽  
Vytas Bindokas ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Chick Embryo ◽  
Neural Cell ◽  
Wild Type ◽  
Mutant Sod1

scholarly journals THE CULTIVATION OF TISSUES FOR PROLONGED PERIODS IN SINGLE FLASKS

1936 ◽  
Vol 64 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Raymond C. Parker
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Connective Tissue ◽  
Breast Muscle ◽  
Cell Multiplication ◽  
Tyrode Solution ◽  
Low Level ◽  
Further Development

1. Fragments of breast muscle from a 12 day old chick embryo have been kept alive in single flasks for an entire year without being transferred. The nutrient materials were supplied by frequent applications of adult fowl serum diluted with Tyrode solution. 2. When fragments of fixed tissues are cultivated in serum, cell multiplication and cell death are both reduced to an extremely low level. 3. The presence of a plasma coagulum is not essential to the continued survival and further development of tissues cultivated inserum. 4. The fibrinogen, prothrombin, and fibrin of coagulated plasma are not essential to the development of connective tissue fibers in vitro.

scholarly journals Regulation of programmed cell death during neural induction in the chick embryo

2011 ◽  
Vol 55 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Anna Gibson ◽  
Neil Robinson ◽  
Andrea Streit ◽  
Guojun Sheng ◽  
Claudio D. Stern
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Programmed Cell Death ◽  
Neural Induction

scholarly journals Muscle cell death during the development of head and neck muscles in the chick embryo

1995 ◽  
Vol 202 (4) ◽  
pp. 365-377 ◽  
Author(s):  
Deedra McClearn ◽  
Richard Medville ◽  
Drew Noden
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Head And Neck ◽  
Muscle Cell ◽  
Neck Muscles
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