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Open AccessJournal ArticleDOI

Enhanced Ca2+-dependent glutamate release from astrocytes of the BACHD Huntington’s disease mouse model

TLDR
This work identifies a new mechanism in astrocytes that could lead to increased levels of extracellular glutamate in HD and thus may contribute to excitotoxicity in this devastating disease.
About
This article is published in Neurobiology of Disease.The article was published on 2013-10-01 and is currently open access. It has received 69 citations till now. The article focuses on the topics: Astrocyte & Excitotoxicity.

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Citations
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Journal ArticleDOI

Astrocyte Calcium Signaling: The Third Wave

TL;DR: The discovery that transient elevations of calcium concentration occur in astrocytes, and release 'gliotransmitters' which act on neurons and vascular smooth muscle, led to the idea that astroCytes are powerful regulators of neuronal spiking, synaptic plasticity and brain blood flow.
Book ChapterDOI

Activation of Astrocytes in Neurodegenerative Diseases

TL;DR: Reversible C(6)F(5) transfer takes place between the boron centers in the anion formed by methide abstraction from [MeZr{N(SiMe(3))(2)}(3)] or [Cp(2)ZrMe(2)] by the perfluorinated diborane 1.
Journal ArticleDOI

Elusive roles for reactive astrocytes in neurodegenerative diseases.

TL;DR: It is aimed to show that the detailed study of reactive astrocytes may open new perspectives for neurodegenerative diseases (ND), and to consider the anticipated developments in this important field.
Journal ArticleDOI

Astrocytes in Neurodegenerative Disease

TL;DR: The role of astrocytes in neurodegenerative diseases is reviewed, focusing on their dysfunction in Huntington's disease, Parkinson's disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS).
References
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Journal ArticleDOI

A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes

TL;DR: In this article, the authors used haplotype analysis of linkage disequilibrium to spotlight a small segment of 4p16.3 as the likely location of the defect, which is expanded and unstable on HD chromosomes.
Journal ArticleDOI

Neuropathological classification of Huntington's disease.

TL;DR: These studies indicate that analyses of the caudate nucleus in grade 4 would reflect mainly its astrocytic composition with a component of remote neurons projecting to the striatum, which would reflect early cellular and biochemical changes in HD.
Journal ArticleDOI

Tripartite synapses : Glia, the unacknowledged partner

TL;DR: It is suggested that perisynaptic Schwann cells and synaptically associated astrocytes should be viewed as integral modulatory elements of tripartite synapses.
Journal ArticleDOI

Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid

TL;DR: It is demonstrated that lesions due to quinolinic acid closely resemble those of HD as they result in marked depletions of both GABA and substance P, with selective sparing of somatostatin/neuropeptide Y neurones.
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