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

Neuron

Volumn 33, Issue 6, 2002, Pages 849-860

  Zeron, Melinda M ^a   Hansson, Oskar ^b   Chen, Nansheng ^a   Wellington, Cheryl L ^c   Leavitt, Blair R ^c   Brundin, Patrik ^b   Hayden, Michael R ^c   Raymond, Lynn A ^a,c,d  

^a Department of Psychiatry   (Sweden)

^b LUND UNIVERSITY   (Sweden)

^c Department of Medical Genetics ^*  (Canada)

^d UNIVERSITY OF BRITISH COLUMBIA   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

AMPA RECEPTOR; CASPASE 3; HUNTINGTIN; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; N METHYL DEXTRO ASPARTIC ACID RECEPTOR BLOCKING AGENT; N METHYL DEXTRO ASPARTIC ACID RECEPTOR STIMULATING AGENT; QUINOLINIC ACID; RECEPTOR SUBUNIT;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CELL CULTURE; CELL DEATH; CELL TYPE; CONTROLLED STUDY; DRUG CYTOTOXICITY; ENZYME ACTIVATION; ENZYME ACTIVITY; GRANULE CELL; HUNTINGTON CHOREA; MOUSE; NERVE CELL; NERVE CELL DEGENERATION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; TRANSGENIC MOUSE; WILD TYPE;

EID: 0037075624     PISSN: 08966273     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0896-6273(02)00615-3     Document Type: Article

References (64)

1. Abnormalities of striatal projection neurons and N-methyl-D-aspartate receptors in presymptomatic Huntington's disease
2. Mechanisms of excitotoxicity in neurological diseases
3. Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
4. AMPA receptor desensitization predicts the selective vulnerability of cerebellar Purkinje cells to excitotoxicity
5. Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons
6. Intrinsic membrane properties of neostriatal neurons can account for their low level of spontaneous activity
7. Synaptic transmission in the striatum: From plasticity to neurodegeneration
8. Dopamine and N-methyl-D-aspartate receptor interactions in the neostriatum
9. NMDA receptor function in mouse models of Huntington disease
10. Differential sensitivity of medium- and large-sized striatal neurons to NMDA but not kainate receptor activation in the rat
11. Differential sensitivity of recombinant N-methyl-D-aspartate receptor subtypes to zinc inhibition
12. Subtype-specific enhancement of NMDA receptor currents by mutant huntingtin
13. Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease
14. Glutamate neurotoxicity and diseases of the nervous system
15. A one-hit model of cell death in inherited neuronal degenerations
16. Truncated N-terminal fragments of huntingtin with expanded glutamine repeats form nuclear and cytoplasmic aggregates in cell culture
17. Lesion of striatal neurones with kainic acid provides a model for Huntington's chorea
18. Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation
19. Excitotoxic injury of the neostriatum: A model for Huntington's disease
20. Selective sparing of a class of striatal neurons in Huntington's disease
21. Inhibition of succinate dehydrogenase by malonic acid produces an "excitotoxic" lesion in rat striatum
22. Nuclear and neuropil aggregates in Huntington's disease: Relationship to neuropathology
23. The influence of huntingtin pore size on nuclear localization and cellular toxicity
24. Transgenic mice expressing a Huntington's disease mutation are resistant to quinolinic acid-induced striatal excitotoxicity
25. Resistance to NMDA toxicity correlates with appearance of nuclear inclusions, behavioural deficits and changes in calcium homeostasis in mice transgenic for exon 1 of the huntington gene
26. A primate model of Huntington's disease: Behavioral and anatomical studies of unilateral excitotoxic lesions of the caudate-putamen in the baboon
27. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes
28. A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration
29. Cloned glutamate receptors
30. Muscarinic receptors modulate N-, P-, and L-type Ca2+ currents in rat striatal neurons through parallel pathways
31. Caspase 3-cleaved N-terminal fragments of wild-type and mutant huntingtin are present in normal and Huntington's disease brains, associate with membranes, and undergo calpain-dependent proteolysis
32. Cortical and striatal neuronal cultures of the same embryonic origin show intrinsic differences in glutamate receptor expression and vulnerability to excitotoxicity
33. Localization of alternatively spliced NMDAR1 glutamate receptor isoforms in rat striatal neurons
34. Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington's disease
35. NMDA receptor subunit mRNA expression by projection neurons and interneurons in rat striatum
36. Enhanced sensitivity to N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease
37. Cellular defects and altered gene expression in PC12 cells stably expressing mutant huntingtin
38. Amino-terminal fragments of mutant huntingtin show selective accumulation in striatal neurons and synaptic toxicity
39. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice
40. Length of huntingtin and its polyglutamine tract influences localization and frequency of intracellular aggregates
41. Duplication of biochemical changes of Huntington's chorea by intrastriatal injections of glutamic and kainic acids
42. Developmental and regional expression in the rat brain and functional properties of four NMDA receptors
43. Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease
44. N-methyl-D-aspartate receptor proteins NR2A and NR2B are differentially distributed in the developing rat central nervous system as revealed by subunit-specific antibodies
45. Caspase-8 is required for cell death induced by expanded polyglutamine repeats
46. Axonal transport of N-terminal huntingtin suggests early pathology of corticostriatal projections in Huntington disease
47. Activation and desensitization of N-methyl-D-aspartate receptors in nucleated outside-out patches from mouse neurones
48. Postsynaptic organization and regulation of excitatory synapses
49. Fluoro-Jade: A novel fluorochrome for the sensitive and reliable histochemical localization of neuronal degeneration
50. Polyglutamine-expanded huntingtin promotes sensitization of N-methyl-D-aspartate receptors via post-synaptic density 95
51. Immunohistochemical localization of N-methyl-D-aspartate receptor NR1, NR2A, NR2B and NR2C/D subunits in the adult mammalian cerebellum
52. Huntington's disease: The challenge for cell biologists
53. The pathways of cell death: Oncosis, apoptosis, and necrosis
54. Neuronal activity differentially regulates NMDA receptor subunit expression in cerebellar granule cells
55. Huntington disease
56. Phosphorylation and modulation of a kainate receptor (GluR6) by camp-dependent protein kinase
57. Modulation of AMPA/kainate receptors in cultured murine hippocampal neurones by protein kinase C
58. Caspases and neurodegeneration: On the cutting edge of new therapeutic approaches
59. Inhibiting caspase cleavage of huntingtin reduces toxicity and aggregate formation in neuronal and nonneuronal cells
60. Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator
61. Ifenprodil discriminates subtypes of the N-methyl-D-aspartate receptor: Selectivity and mechanisms at recombinant heteromeric receptors
62. NMDA receptor losses in putamen from patients with Huntington's disease
63. Mutant huntingtin enhances excitotoxic cell death