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Neonatal mice of the down syndrome model, Ts65Dn, exhibit upregulated VIP measures and reduced responsiveness of cortical astrocytes to VIP stimulation

Overview of attention for article published in Journal of Molecular Neuroscience, January 2006
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Title
Neonatal mice of the down syndrome model, Ts65Dn, exhibit upregulated VIP measures and reduced responsiveness of cortical astrocytes to VIP stimulation
Published in
Journal of Molecular Neuroscience, January 2006
DOI 10.1385/jmn:30:3:329
Pubmed ID
Authors

Nadia Sahir, Douglas E. Brenneman, Joanna M. Hill

Abstract

The Ts65Dn segmental mouse model of Down syndrome (DS) possesses a triplication of the section of chromosome 16 that is most homologous to the human chromosome 21 that is trisomic in DS. This model exhibits many of the characteristics of DS including small size, developmental delays, and a decline of cholinergic systems and cognitive function with age. Recent studies have shown that vasoactive intestinal peptide (VIP) systems are upregulated in aged Ts65Dn mice and that VIP dysregulation during embryogenesis is followed by the hypotonia and developmental delays as seen in both DS and in Ts65Dn mice. Additionally, astrocytes from aged Ts65Dn brains do not respond to VIP stimulation to release survival-promoting substances. To determine if VIP dysregulation is age-related in Ts65Dn mice, the current study examined VIP and VIP receptors (VPAC-1 and VPAC-2) in postnatal day 8 Ts65Dn mice. VIP and VPAC-1 expression was significantly increased in the brains of trisomic mice compared with wild-type mice. VIP-binding sites were also significantly increased in several brain areas of young Ts65Dn mice, especially in the cortex, caudate/putamen, and hippocampus. Further, in vitro treatment of normal neurons with conditioned medium from VIP-stimulated Ts65Dn astrocytes from neonatal mice did not enhance neuronal survival. This study indicates that VIP anomalies are present in neonatal Ts65Dn mice, a defect occurs in the signal transduction mechanism of the VPAC-1 VIP receptor, cortical astrocytes from neonatal brains are dysfunctional, and further, that VIP dysregulation may play a significant role in DS.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 6%
Spain 1 6%
Unknown 16 89%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 39%
Researcher 5 28%
Professor > Associate Professor 2 11%
Student > Master 2 11%
Student > Bachelor 1 6%
Other 1 6%
Readers by discipline Count As %
Agricultural and Biological Sciences 4 22%
Neuroscience 4 22%
Medicine and Dentistry 3 17%
Psychology 3 17%
Nursing and Health Professions 1 6%
Other 3 17%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 August 2012.
All research outputs
#22,759,452
of 25,373,627 outputs
Outputs from Journal of Molecular Neuroscience
#1,330
of 1,643 outputs
Outputs of similar age
#170,045
of 174,007 outputs
Outputs of similar age from Journal of Molecular Neuroscience
#15
of 17 outputs
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We're also able to compare this research output to 17 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.