scholarly journals Deficiency of Pro-apoptotic Hrk Attenuates Programmed Cell Death in the Developing Murine Nervous System but Does Not Affect Bcl-x Deficiency-Induced Neuron Apoptosis

2011 ◽  
Vol 59 (11) ◽  
pp. 976-983 ◽  
Author(s):  
Arindam P. Ghosh ◽  
Jennifer D. Cape ◽  
Barbara J. Klocke ◽  
Kevin A. Roth
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
System Development ◽  
Critical Role ◽  
Family Members ◽  
Nervous System Development ◽  
Neuronal Populations ◽  
Embryonic Nervous System ◽  
Induced Neuron

The BCL-2 family includes both pro- and anti-apoptotic proteins, which regulate programmed cell death during development and in response to various apoptotic stimuli. The BH3-only subgroup of pro-apoptotic BCL-2 family members is critical for the induction of apoptotic signaling, by binding to and neutralizing anti-apoptotic BCL-2 family members. During embryonic development, the anti-apoptotic protein BCL-XL plays a critical role in the survival of neuronal populations by regulating the multi-BH domain protein BAX. In this study, the authors investigated the role of Harakiri (HRK), a relatively recently characterized BH3-only molecule in disrupting the BAX-BCL-XL interaction during nervous system development. Results indicate that HRK deficiency significantly reduces programmed cell death in the nervous system. However, HRK deficiency does not significantly attenuate the widespread apoptosis seen in the Bcl-x−/− embryonic nervous system, indicating that other BH3-only molecules, alone or in combination, may regulate BAX activation in immature neurons.

Programmed Cell Death During Nervous System Development

2009 ◽  
Author(s):  
Mark S. Blumberg ◽  
John H. Freeman ◽  
Scott R. Robinson ◽  
Ronald W. Oppenheim ◽  
Carol Milligan ◽  
...  
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
System Development ◽  
Nervous System Development

scholarly journals RNA interference screen to identify genes required for Drosophila embryonic nervous system development

2007 ◽  
Vol 104 (13) ◽  
pp. 5626-5631 ◽  
Author(s):  
K. Koizumi ◽  
H. Higashida ◽  
S. Yoo ◽  
M. S. Islam ◽  
A. I. Ivanov ◽  
...  
Keyword(s):  
Nervous System ◽  
Rna Interference ◽  
System Development ◽  
Nervous System Development ◽  
Embryonic Nervous System

Inhibition of cell death results in hyperganglionosis: implications for enteric nervous system development

2009 ◽  
Vol 21 (7) ◽  
pp. 768-e49 ◽  
Author(s):  
a. s. wallace ◽  
a. j. barlow ◽  
l. navaratne ◽  
j-m. delalande ◽  
s. tauszig-delamasure ◽  
...  
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Enteric Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Enteric Nervous System Development

scholarly journals Interaction Between the Complement System and Infectious Agents – A Potential Mechanistic Link to Neurodegeneration and Dementia

2021 ◽  
Vol 15 ◽  
Author(s):  
Noriko Shinjyo ◽  
Wataru Kagaya ◽  
Marcela Pekna
Keyword(s):  
Nervous System ◽  
Complement System ◽  
Complement Activation ◽  
Neural Plasticity ◽  
Measles Virus ◽  
System Development ◽  
Critical Role ◽  
Nervous System Development ◽  
Infectious Agents ◽  
The Complement System

As part of the innate immune system, complement plays a critical role in the elimination of pathogens and mobilization of cellular immune responses. In the central nervous system (CNS), many complement proteins are locally produced and regulate nervous system development and physiological processes such as neural plasticity. However, aberrant complement activation has been implicated in neurodegeneration, including Alzheimer’s disease. There is a growing list of pathogens that have been shown to interact with the complement system in the brain but the short- and long-term consequences of infection-induced complement activation for neuronal functioning are largely elusive. Available evidence suggests that the infection-induced complement activation could be protective or harmful, depending on the context. Here we summarize how various infectious agents, including bacteria (e.g., Streptococcus spp.), viruses (e.g., HIV and measles virus), fungi (e.g., Candida spp.), parasites (e.g., Toxoplasma gondii and Plasmodium spp.), and prion proteins activate and manipulate the complement system in the CNS. We also discuss the potential mechanisms by which the interaction between the infectious agents and the complement system can play a role in neurodegeneration and dementia.

scholarly journals Noninvasive harmonics optical microscopy for long-term observation of embryonic nervous system development in vivo

2006 ◽  
Vol 11 (5) ◽  
pp. 054022 ◽  
Author(s):  
Szu-Yu Chen ◽  
Cho-Shuen Hsieh ◽  
Shi-Wei Chu ◽  
Cheng-Yung Lin ◽  
Ching-Yi Ko ◽  
...  
Keyword(s):  
Nervous System ◽  
Optical Microscopy ◽  
System Development ◽  
Nervous System Development ◽  
Embryonic Nervous System ◽  
Long Term Observation

scholarly journals Spatiotemporal expression of IgLON family members in the developing mouse nervous system

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sydney Fearnley ◽  
Reesha Raja ◽  
Jean-François Cloutier
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Developmental Disorders ◽  
System Development ◽  
Expression Patterns ◽  
Family Members ◽  
Autism Spectrum ◽  
Nervous System Development ◽  
Spatiotemporal Expression ◽  
Developing Nervous System

AbstractDifferential expression of cell adhesion molecules in neuronal populations is one of the many mechanisms promoting the formation of functional neural circuits in the developing nervous system. The IgLON family consists of five cell surface immunoglobulin proteins that have been associated with various developmental disorders, such as autism spectrum disorder, schizophrenia, and major depressive disorder. However, there is still limited and fragmented information about their patterns of expression in certain regions of the developing nervous system and how their expression contributes to their function. Utilizing an in situ hybridization approach, we have analyzed the spatiotemporal expression of all IgLON family members in the developing mouse brain, spinal cord, eye, olfactory epithelium, and vomeronasal organ. At one prenatal (E16) and two postnatal (P0 and P15) ages, we show that each IgLON displays distinct expression patterns in the olfactory system, cerebral cortex, midbrain, cerebellum, spinal cord, and eye, indicating that they likely contribute to the wiring of specific neuronal circuitry. These analyses will inform future functional studies aimed at identifying additional roles for these proteins in nervous system development.

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