scholarly journals Apoptotic Cell Death Following Traumatic Injury to the Central Nervous System

BMB Reports ◽  
2002 ◽  
Vol 35 (1) ◽  
pp. 94-105 ◽  
Author(s):  
Joe E. Springer
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Apoptotic Cell ◽  
Traumatic Injury ◽  
Apoptotic Cell Death ◽  
The Central Nervous System

Apoptotic cell death in the central nervous system of Bufo arenarum tadpoles induced by cypermethrin

2006 ◽  
Vol 22 (3) ◽  
pp. 199-211 ◽  
Author(s):  
V. H. Casco ◽  
M. F. Izaguirre ◽  
L. Marín ◽  
M. N. Vergara ◽  
R. C. Lajmanovich ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Bufo Arenarum ◽  
The Central Nervous System

Two Types of Apoptotic Cell Death of Rat Central Nervous System-Derived Neuroblastoma B50 and B104 Cells: Apoptosis Induced During Proliferation and After Differentiation

2002 ◽  
Vol 67 (5) ◽  
pp. 1856-1865 ◽  
Author(s):  
Naoyuki Honma ◽  
Atsuko Uchida ◽  
Hiroya Hirose ◽  
Vlastimil Srsen ◽  
Takeo Kishimoto ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

scholarly journals Mutations affecting neural survival in the zebrafish Danio rerio

Development ◽  
1996 ◽  
Vol 123 (1) ◽  
pp. 217-227 ◽  
Author(s):  
S. Abdelilah ◽  
E. Mountcastle-Shah ◽  
M. Harvey ◽  
L. Solnica-Krezel ◽  
A.F. Schier ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
Danio Rerio ◽  
Apoptotic Cell ◽  
Brain Morphology ◽  
Genetic Components ◽  
The Central Nervous System ◽  
Dying Cells

Programmed cell death is a prominent feature of normal animal development. During neurogenesis, naturally occurring cell death is a mechanism to eliminate neurons that fail to make appropriate connections. To prevent accidental cell death, mechanisms that trigger programmed cell death, as well as the genetic components of the cell death program, are tightly controlled. In a large-scale mutagenesis screen for embryonic lethal mutations in zebrafish Danio rerio we have found 481 mutations with a neural degeneration phenotype. Here, we present 50 mutations that fall into two classes (termed spacehead and fala-like) that are characterized by two main features: first, they appear to affect cell survival primarily within the neuroectodermal lineages during somitogenesis, and second, they show an altered brain morphology at or before 28 hours of development. Evidence for the specificity of cell death within the central nervous system comes from visual inspection of dying cells and analysis of DNA fragmentation, a process associated with apoptotic cell death. In mutants, the level of dying cells is significantly increased in brain and spinal cord. Furthermore, at the end of somitogenesis, the cell count of radial glia and trigeminal neurons is reduced in some mutants of the spacehead class. A variety of neurodegenerative disorders in mouse and humans have been associated with abnormal levels of programmed cell death within the central nervous system. The mutations presented here might provide a genetic framework to aid in the understanding of the etiology of degenerative and physiological disorders within the CNS and the activation of inappropriate programmed cell death.

Understanding Neuropathic Pain

CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Neuronal Excitability ◽  
Traumatic Injury ◽  
Nerve Fibers ◽  
Cellular Events ◽  
Excitatory Neurotransmitters ◽  
The Central Nervous System ◽  
Activity Dependent

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.

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