Ethanol exposure alters neurotrophin receptor expression in the rat central nervous system: Effects of neonatal exposure

2004 ◽  
Vol 60 (1) ◽  
pp. 114-126 ◽  
Author(s):  
D. Blaine Moore ◽  
Irina Madorsky ◽  
Michael Paiva ◽  
Marieta Barrow Heaton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ethanol Exposure ◽  
Receptor Expression ◽  
Neurotrophin Receptor ◽  
Neonatal Exposure

An optimised procedure for prenatal ethanol exposure with determination of its effects on central nervous system connections

1999 ◽  
Vol 3 (3) ◽  
pp. 264-269 ◽  
Author(s):  
Alessandro Sbriccoli ◽  
Donatella Carretta ◽  
Marialaura Santarelli ◽  
Alberto Granato ◽  
Diego Minciacchi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure

scholarly journals Expression of the Mouse Hepatitis Virus Receptor by Central Nervous System Microglia

2004 ◽  
Vol 78 (14) ◽  
pp. 7828-7832 ◽  
Author(s):  
Chandran Ramakrishna ◽  
Cornelia C. Bergmann ◽  
Kathryn V. Holmes ◽  
Stephen A. Stohlman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hepatitis Virus ◽  
Acute Infection ◽  
Mouse Hepatitis Virus ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Receptor Expression ◽  
Down Regulation ◽  
Virus Receptor

ABSTRACT Detection of the mouse hepatitis virus receptor within the central nervous system (CNS) has been elusive. Receptor expression on microglia was reduced during acute infection and restored following immune-mediated virus control. Receptor down regulation was independent of neutrophils, NK cells, gamma interferon, or perforin. Infection of mice devoid of distinct inflammatory cells revealed CD4+ T cells as the major cell type influencing receptor expression by microglia. In addition to demonstrating receptor expression on CNS resident cells, these data suggest that transient receptor down regulation on microglia aids in establishing persistence in the CNS by assisting virus infection of other glial cell types.

scholarly journals Systemic Central Nervous System (CNS)-targeted Delivery of Neuropeptide Y (NPY) Reduces Neurodegeneration and Increases Neural Precursor Cell Proliferation in a Mouse Model of Alzheimer Disease

2015 ◽  
Vol 291 (4) ◽  
pp. 1905-1920 ◽  
Author(s):  
Brian Spencer ◽  
Rewati Potkar ◽  
Jeff Metcalf ◽  
Ivy Thrin ◽  
Anthony Adame ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Alzheimer Disease ◽  
Mouse Model ◽  
Neuropeptide Y ◽  
Targeted Delivery ◽  
Lentiviral Vector ◽  
Receptor Expression ◽  
Neural Precursor ◽  
The Central Nervous System

Neuropeptide Y (NPY) is one of the most abundant protein transmitters in the central nervous system with roles in a variety of biological functions including: food intake, cardiovascular regulation, cognition, seizure activity, circadian rhythms, and neurogenesis. Reduced NPY and NPY receptor expression is associated with numerous neurodegenerative disorders including Alzheimer disease (AD). To determine whether replacement of NPY could ameliorate some of the neurodegenerative and behavioral pathology associated with AD, we generated a lentiviral vector expressing NPY fused to a brain transport peptide (apoB) for widespread CNS delivery in an APP-transgenic (tg) mouse model of AD. The recombinant NPY-apoB effectively reversed neurodegenerative pathology and behavioral deficits although it had no effect on accumulation of Aβ. The subgranular zone of the hippocampus showed a significant increase in proliferation of neural precursor cells without further differentiation into neurons. The neuroprotective and neurogenic effects of NPY-apoB appeared to involve signaling via ERK and Akt through the NPY R1 and NPY R2 receptors. Thus, widespread CNS-targeted delivery of NPY appears to be effective at reversing the neuronal and glial pathology associated with Aβ accumulation while also increasing NPC proliferation. Overall, increased delivery of NPY to the CNS for AD might be an effective therapy especially if combined with an anti-Aβ therapeutic.

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