Increased sensitivity to N-methyl-D-aspartate receptor-mediated excitotoxicity in a mouse model of Huntington's disease.

By Melinda M. Zeron, Oskar Hansson, N. Chen, C. Wellington, B. Leavitt, P. Brundin, Michael R. Hayden, L. Raymond. Neuron, 2002

639 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a98f90cb39b5766e03140e8607863e8d91c54a0c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Sovan Sarkar
2. C. Zuccato
3. E. Cattaneo
4. Cahir O'Kane
5. M. Valenza
6. D. Rubinsztein
7. P. Maher
8. Jana Lewerenz

In Molecular Biology

1. M. Valenza
2. E. Cattaneo
3. P. Maher
4. Jana Lewerenz
5. C. Zuccato
6. D. Rubinsztein
7. N. Mizushima
8. M. Jäättelä

Citations in the corpus

• Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice (2008, result): “…is consistent with previous studies revealing early dysfunction in cortical inputs and NMDA receptors in striatal neurons long before the onset of neurodegenerative changes in a variety of HD mouse models (Levine et al., 1999; Cepeda et al., 2001, 2003; Zeron et al., 2002; Starling et al., 2005).”
• Normal huntingtin function: an alternative approach to Huntington's disease (2005, background): “, to which cells are made more susceptible by the full-length mutant protei”
• Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines (2002, result): “Our results indicate that striatal neurons receiving glutamatergic input via NMDA receptors should show exaggerated cytosolic Ca 2+ responses and excessive mitochondrial depolarization; recent results confirm these prediction”
• Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway (2008, background): “Virgin female flies of the genotype y w; gmr-httNterm(1-171)Q120 (gmrQ120)(22) were allowed to mate with male flies from an isogenised w(1118) stock(23) in food vials for 48 h.”
• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “Thus the presence of NR2B-type NMDAR complex with impaired functional characteristics may help to explain the preferential vulnerability of these cells in HD (132, 658).”
• Cleavage at the caspase-6 site is required for neuronal dysfunction and degeneration due to mutant huntingtin. (2006, methodology): “Overactivation of glutamate receptors has been considered a fundamental underlying mechanism in the early stages of HD (Beal et al., 1986; Albin et al., 1990; Levine et al., 1999; Zeron et al., 2002).”
• Chronic Glutamate Toxicity in Neurodegenerative Diseases—What is the Evidence? (2015, background): “Moreover, NMDA receptormediated currents in MSN were demonstrated to be largely sensitive to the NR2B-specific inhibitor ifenprodil (Zeron et al., 2002).”