Lithium suppresses excitotoxicity-induced striatal lesions in a rat model of Huntington's disease

Neuroscience

Volumn 106, Issue 3, 2001, Pages 603-612

  Wei, H ^a   Qin, Z H ^b   Senatorov, V V ^a   Wei, W ^a   Wang, Y ^b   Qian, Y ^a   Chuang, D M ^a  

^a NATIONAL INSTITUTE OF MENTAL HEALTH   (United States)

^b NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE   (United States)

Author keywords

Bcl 2; Neurodegenerative diseases; Neuroprotection; Quinolinic acid; Striatum

Indexed keywords

BIOTIN; DNA NUCLEOTIDYLEXOTRANSFERASE; LITHIUM; LITHIUM CHLORIDE; PROTEIN BCL 2; QUINOLINIC ACID;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN INJURY; CELL LABELING; CONCENTRATION RESPONSE; CONTROLLED STUDY; CORPUS STRIATUM; DRUG INFUSION; HUNTINGTON CHOREA; IMMUNOBLOTTING; IMMUNOHISTOCHEMISTRY; MALE; NERVE CELL; NEUROPROTECTION; NICK END LABELING; NONHUMAN; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; RAT;

(R)-2,3,4,5-TETRAHYDRO-8-CHLORO-3-METHYL-5-PHENYL-1H-3-BENZAZEPIN-7-OL; ANIMALS; ANTIMANIC AGENTS; CELL DEATH; CYCLIN D1; DISEASE MODELS, ANIMAL; DOPAMINE ANTAGONISTS; GLUTAMATE DECARBOXYLASE; HUNTINGTON DISEASE; IMMUNOHISTOCHEMISTRY; IN SITU NICK-END LABELING; ISOENZYMES; LITHIUM; LITHIUM CHLORIDE; MALE; NEOSTRIATUM; NEURONS; NEUROPROTECTIVE AGENTS; NEUROTOXINS; QUINOLINIC ACID; RADIOLIGAND ASSAY; RATS; RATS, SPRAGUE-DAWLEY; RECEPTORS, DOPAMINE D1; RNA, MESSENGER;

EID: 0035960005     PISSN: 03064522     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0306-4522(01)00311-6     Document Type: Article

References (42)

1. The Bcl-2 protein family: Arbiters of cell survival
2. Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
3. Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons
4. Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity
5. The mood-stabilizing agents lithium and valproate robustly increase the levels of the neuroprotective protein bcl-2 in the CNS
6. Cerebral hypoxia - Some new approaches and unanswered questions
7. Excitotoxic cell death
8. Oxidative stress, glutamate, and neurodegenerative disorders
9. Lesion of striatal neurons with kainic acid provides a model for Huntington's chorea
10. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
11. Morphometric demonstration of atrophic changes in the cerebral cortex, white matter, and neostriatum in Huntington's disease
12. Excitotoxic injury of the neostriatum: A model for Huntington's disease
13. Lithium acutely inhibits and chronically up-regulates and stabilizes glutamate uptake by presynaptic nerve endings in mouse cerebral cortex
14. Neuronal loss in layers V and VI of cerebral cortex in Huntington's disease
15. 2 dopamine receptor proteins in the dorsal striatum and their synaptic relationships with motor corticostriatal afferents
16. L interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation
17. A novel gene containing a trinucleotide repeat that is expanded and unstable on HD chromosome
18. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
19. NMDA receptor subunit mRNA expression by projection neurons and interneurons in rat striatum
20. Quantitative assessment of quinolinic acid-induced striatal toxicity in rats using radioligand binding assays
21. Duplication of biochemical changes of Huntington's chorea by intrastriatal injections of glutamic and kainic acids
22. Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats
23. Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx
24. Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease
25. A protective effect of lithium on rat behaviour altered by ibotenic acid lesions of the basal forebrain cholinergic system
26. Evidence for apoptotic cell death in Huntington disease and excitotoxic animal models
27. Dopaminergic and glutamatergic blocking drugs differentially regulate gene expression of glutamic acid decarboxylase in mouse brain
28. Stimulation of N-methyl-D-aspartate receptors induces apoptosis in rat brain
29. Nuclear factor-κB contributes to excitotoxin-induced apoptosis in rat striatum
30. Nuclear factor κB nuclear translocation upregulates c-Myc and p53 expression during NMDA receptor-mediated apoptosis in rat striatum
31. Selective loss of glial glutamate transporter GLT-1 in amyotrophic lateral sclerosis
32. Quinolinic acid: An endogenous metabolite that produces axon-sparing lesions in rat brain
33. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
34. Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway
35. Effects of chronic lithium treatment on ornithine decarboxylase induction and excitotoxic morphology in the rat
36. Bcl-2 inhibits the mitochondrial release of an apoptogenic protease
37. 1 mutants linked to amyotrophic lateral sclerosis selectively inactivate a glial glutamate transporter
38. Neuropathological classification of Huntington's disease
39. Co-stimulation of cyclic AMP-linked metabotropic glutamate receptors in rat striatum attenuates excitotoxin-induced NF-κB activation and apoptosis
40. + efflux and neuronal apoptosis
41. MK-801 prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism in primates