scholarly journals Local Type I IFN Receptor Signaling Protects against Virus Spread within the Central Nervous System

2009 ◽  
Vol 182 (4) ◽  
pp. 2297-2304 ◽  
Author(s):  
Claudia N. Detje ◽  
Thomas Meyer ◽  
Hauke Schmidt ◽  
Dorothea Kreuz ◽  
John K. Rose ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Type I ◽  
Receptor Signaling ◽  
Type I Ifn ◽  
Virus Spread ◽  
Local Type ◽  
The Central Nervous System

Crosstalk Between Insulin and Toll-like Receptor Signaling Pathways in the Central Nervous system

2014 ◽  
Vol 50 (3) ◽  
pp. 797-810 ◽  
Author(s):  
Fatemeh Hemmati ◽  
Rasoul Ghasemi ◽  
Norlinah Mohamed Ibrahim ◽  
Leila Dargahi ◽  
Zahurin Mohamed ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Signaling Pathways ◽  
Receptor Signaling ◽  
Toll Like Receptor ◽  
The Central Nervous System

scholarly journals Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleotide Metabolism ◽  
Neural Cells ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Neuroepithelial Cells ◽  
The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

scholarly journals Leptin Receptor Signaling and Action in the Central Nervous System

Obesity ◽  
2006 ◽  
Vol 14 ◽  
pp. 208S-212S ◽  
Author(s):  
Rebecca L. Leshan ◽  
Marie Björnholm ◽  
Heike Münzberg ◽  
Martin G. Myers
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Leptin Receptor ◽  
Receptor Signaling ◽  
The Central Nervous System

Cellular mechanisms of muscle fatigue

1994 ◽  
Vol 74 (1) ◽  
pp. 49-94 ◽  
Author(s):  
R. H. Fitts
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Muscle Fatigue ◽  
Fiber Type ◽  
Type I ◽  
Fiber Types ◽  
Force Frequency ◽  
Frequency Curve ◽  
Tension Development ◽  
The Central Nervous System

Fatigue, defined as the failure to maintain the required or expected power output, is a complex problem, since multiple factors are clearly involved, with the relative importance of each dependent on the fiber type composition of the contracting muscles(s), and the intensity, type, and duration of the contractile activity. The primary sites of fatigue appear to be within the muscle cell itself and for the most part do not involve the central nervous system or the neuromuscular junction. The major hypotheses of fatigue center on disturbances in the surface membrane, E-C coupling, or metabolic events. The cell sites most frequently linked to the etiology of skeletal muscle fatigue are shown in Figure 1. Skeletal muscles are composed of at least four distinct fiber types (3 fast twitch and 1 slow twitch), with the slow type I and fast type IIa fibers containing the highest mitochondrial content and fatigue resistance. Despite fiber type differences in the degree of fatigability, the contractile properties undergo characteristic changes with the development of fatigue that can be observed in whole muscles, single motor units, and single fibers. The Po declines, and the contraction and relaxation times are prolonged. Additionally, there is a decrease in the peak rate of tension development and decline and a reduced Vo. Changes in Vo are more resistant to fatigue than Po and are not observed until Po has declined by at least 10% of its initial prefatigued value. However, the reduced peak power by which fatigue is defined results from both a reduction in Vo and Po. In the absence of muscle fiber damage, the prolonged relaxation time associated with fatigue causes the force-frequency curve to shift to the left, such that peak tensions are obtained at lower frequencies of stimulation. In a mechanism not clearly understood, the central nervous system senses this condition and reduces the alpha-motor nerve activation frequency as fatigue develops. In some cases, selective LFF develops that displaces the force-frequency curve to the right. Although not proven, it appears likely that this condition is associated with and likely caused by muscle injury, such that the SR releases less Ca2+ at low frequencies of activation. Alternatively, LFF could result from a reduced membrane excitability, such that the sarcolemma action potential frequency is considerably less than the stimulation frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

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