Glutamate Uptake is Reduced in Prefrontal Cortex in Huntington’s Disease

2007 ◽  
Vol 33 (2) ◽  
pp. 232-237 ◽  
Author(s):  
Bjørnar Hassel ◽  
Shoshi Tessler ◽  
Richard L. M. Faull ◽  
Piers C. Emson
Keyword(s):  
Prefrontal Cortex ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Glutamate Uptake

scholarly journals Diffusion weighted imaging of prefrontal cortex in prodromal huntington's disease

2013 ◽  
Vol 35 (4) ◽  
pp. 1562-1573 ◽  
Author(s):  
Joy T. Matsui ◽  
Jatin G. Vaidya ◽  
Hans J. Johnson ◽  
Vincent A. Magnotta ◽  
Jeffrey D. Long ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Diffusion Weighted Imaging ◽  
Diffusion Weighted

Morphometric analysis of the prefrontal cortex in Huntington's disease

Neurology ◽  
1991 ◽  
Vol 41 (7) ◽  
pp. 1117-1117 ◽  
Author(s):  
A. Sotrel ◽  
P. A. Paskevich ◽  
D. K. Kiely ◽  
E. D. Bird ◽  
R. S. Williams ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Morphometric Analysis

scholarly journals Early dysfunction and progressive degeneration of the subthalamic nucleus in mouse models of Huntington's disease

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Jeremy F Atherton ◽  
Eileen L McIver ◽  
Matthew RM Mullen ◽  
David L Wokosin ◽  
D James Surmeier ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Mouse Models ◽  
Subthalamic Nucleus ◽  
Glutamate Uptake ◽  
Oxidant Stress ◽  
Katp Channels ◽  
Receptor Antagonism ◽  
Progressive Degeneration

The subthalamic nucleus (STN) is an element of cortico-basal ganglia-thalamo-cortical circuitry critical for action suppression. In Huntington's disease (HD) action suppression is impaired, resembling the effects of STN lesioning or inactivation. To explore this potential linkage, the STN was studied in BAC transgenic and Q175 knock-in mouse models of HD. At <2 and 6 months of age autonomous STN activity was impaired due to activation of KATP channels. STN neurons exhibited prolonged NMDA receptor-mediated synaptic currents, caused by a deficit in glutamate uptake, and elevated mitochondrial oxidant stress, which was ameliorated by NMDA receptor antagonism. STN activity was rescued by NMDA receptor antagonism or the break down of hydrogen peroxide. At 12 months of age approximately 30% of STN neurons had been lost, as in HD. Together, these data argue that dysfunction within the STN is an early feature of HD that may contribute to its expression and course.

scholarly journals Up-regulation of GLT1 expression increases glutamate uptake and attenuates the Huntington's disease phenotype in the R6/2 mouse

Neuroscience ◽  
2008 ◽  
Vol 153 (1) ◽  
pp. 329-337 ◽  
Author(s):  
B.R. Miller ◽  
J.L. Dorner ◽  
M. Shou ◽  
Y. Sari ◽  
S.J. Barton ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Glutamate Uptake ◽  
Disease Phenotype

Presymptomatic Glutamate Levels in Prefrontal Cortex in the Hdh(CAG150) Mouse Model of Huntington's Disease

2014 ◽  
Vol 3 (4) ◽  
pp. 387-399 ◽  
Author(s):  
Antigone Wolfram-Aduan ◽  
Megan Altemus ◽  
John H. Wickwire ◽  
Michael I. Sandstrom
Keyword(s):  
Prefrontal Cortex ◽  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease
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