scholarly journals Injury-Induced DNA Replication and Neural Proliferation in the Adult Mammalian Nervous System

10.5772/19107 ◽  
2011 ◽  
Author(s):  
Krzysztof Czaja ◽  
Wioletta E. ◽  
Maria G. ◽  
Stefano Geuna ◽  
Michele Fornaro
Keyword(s):  
Nervous System ◽  
Dna Replication

scholarly journals Protective Mechanisms Against DNA Replication Stress in the Nervous System

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 730
Author(s):  
Clara Forrer Charlier ◽  
Rodrigo A. P. Martins
Keyword(s):  
Dna Damage ◽  
Nervous System ◽  
Dna Replication ◽  
Neurological Diseases ◽  
Replication Stress ◽  
Nervous System Development ◽  
Stress Generation ◽  
Genome Replication ◽  
Cns Development ◽  
Dna Replication Stress

The precise replication of DNA and the successful segregation of chromosomes are essential for the faithful transmission of genetic information during the cell cycle. Alterations in the dynamics of genome replication, also referred to as DNA replication stress, may lead to DNA damage and, consequently, mutations and chromosomal rearrangements. Extensive research has revealed that DNA replication stress drives genome instability during tumorigenesis. Over decades, genetic studies of inherited syndromes have established a connection between the mutations in genes required for proper DNA repair/DNA damage responses and neurological diseases. It is becoming clear that both the prevention and the responses to replication stress are particularly important for nervous system development and function. The accurate regulation of cell proliferation is key for the expansion of progenitor pools during central nervous system (CNS) development, adult neurogenesis, and regeneration. Moreover, DNA replication stress in glial cells regulates CNS tumorigenesis and plays a role in neurodegenerative diseases such as ataxia telangiectasia (A-T). Here, we review how replication stress generation and replication stress response (RSR) contribute to the CNS development, homeostasis, and disease. Both cell-autonomous mechanisms, as well as the evidence of RSR-mediated alterations of the cellular microenvironment in the nervous system, were discussed.

scholarly journals Stress Hormones Epinephrine and Corticosterone Selectively Modulate Herpes Simplex Virus 1 (HSV-1) and HSV-2 Productive Infections in Adult Sympathetic, but Not Sensory, Neurons

2017 ◽  
Vol 91 (13) ◽  
Author(s):  
Angela M. Ives ◽  
Andrea S. Bertke
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Dna Replication ◽  
Herpes Simplex ◽  
Sensory Neurons ◽  
Stress Hormones ◽  
Neuronal Cultures ◽  
Autonomic Neurons ◽  
Viral Progeny ◽  
Hsv 1

ABSTRACT Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) infect and establish latency in peripheral neurons, from which they can reactivate to cause recurrent disease throughout the life of the host. Stress is associated with the exacerbation of clinical symptoms and the induction of recurrences in humans and animal models. The viruses preferentially replicate and establish latency in different subtypes of sensory neurons, as well as in neurons of the autonomic nervous system that are highly responsive to stress hormones. To determine if stress-related hormones modulate productive HSV-1 and HSV-2 infections within sensory and autonomic neurons, we analyzed viral DNA and the production of viral progeny after treatment of primary adult murine neuronal cultures with the stress hormones epinephrine and corticosterone. Both sensory trigeminal ganglion (TG) and sympathetic superior cervical ganglion (SCG) neurons expressed adrenergic receptors (activated by epinephrine) and the glucocorticoid receptor (activated by corticosterone). Productive HSV infection colocalized with these receptors in SCG but not in TG neurons. In productively infected neuronal cultures, epinephrine treatment significantly increased the levels of HSV-1 DNA replication and production of viral progeny in SCG neurons, but no significant differences were found in TG neurons. In contrast, corticosterone significantly decreased the levels of HSV-2 DNA replication and production of viral progeny in SCG neurons but not in TG neurons. Thus, the stress-related hormones epinephrine and corticosterone selectively modulate acute HSV-1 and HSV-2 infections in autonomic, but not sensory, neurons. IMPORTANCE Stress exacerbates acute disease symptoms resulting from HSV-1 and HSV-2 infections and is associated with the appearance of recurrent skin lesions in millions of people. Although stress hormones are thought to impact HSV-1 and HSV-2 through immune system suppression, sensory and autonomic neurons that become infected by HSV-1 and HSV-2 express stress hormone receptors and are responsive to hormone fluctuations. Our results show that autonomic neurons are more responsive to epinephrine and corticosterone than are sensory neurons, demonstrating that the autonomic nervous system plays a substantial role in HSV pathogenesis. Furthermore, these results suggest that stress responses have the potential to differentially impact HSV-1 and HSV-2 so as to produce divergent outcomes of infection.

Assessment of DNA replication in central nervous system by Laser Scanning Cytometry

2004 ◽  
Author(s):  
Dominik Lenz ◽  
Birgit Mosch ◽  
Jozsef Bocsi ◽  
Thomas Arendt ◽  
Attila Tßrnok
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Dna Replication ◽  
Laser Scanning ◽  
Laser Scanning Cytometry

Neurotropic enteroviruses co-opt “fair-weather-friend” commensal gut microbiota to drive host infection and central nervous system disturbances

2019 ◽  
Vol 42 ◽  
Author(s):  
Kevin B. Clark
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gut Bacteria ◽  
Infection Cycle ◽  
Fair Weather ◽  
Host Health ◽  
Microbe Interactions ◽  
Animal Hosts ◽  
Host Infection ◽  
Neuropsychiatric Conditions

Abstract Some neurotropic enteroviruses hijack Trojan horse/raft commensal gut bacteria to render devastating biomimicking cryptic attacks on human/animal hosts. Such virus-microbe interactions manipulate hosts’ gut-brain axes with accompanying infection-cycle-optimizing central nervous system (CNS) disturbances, including severe neurodevelopmental, neuromotor, and neuropsychiatric conditions. Co-opted bacteria thus indirectly influence host health, development, behavior, and mind as possible “fair-weather-friend” symbionts, switching from commensal to context-dependent pathogen-like strategies benefiting gut-bacteria fitness.

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