NMDA receptor-mediated excitotoxicity contributes to the cerebral hypoxic injury of a rat model of posthypoxic myoclonus

Brain Research

Volumn 1133, Issue 1, 2007, Pages 209-215

  Tai, Kwok Keung ^a,b   Truong, Daniel D ^a,b  

^a LONG BEACH MEMORIAL MEDICAL CENTER   (United States)

^b Parkinson's and Movement Disorder Institute   (United States)

Author keywords

Brain injury; Cardiac arrest; Excitotoxicity; Hypoxia; Neurodegeneration; NMDA receptor; Posthypoxic myoclonus

Indexed keywords

ADRENALIN; BICARBONATE; CLONAZEPAM; MEMANTINE; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; VALPROIC ACID;

ADOLESCENT; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN HYPOXIA; CEREBELLUM; CONTROLLED STUDY; EXCITOTOXICITY; HEART ARREST; HIPPOCAMPUS; MALE; MOTOR DYSFUNCTION; MYOCLONUS; NERVE DEGENERATION; NONHUMAN; PRIORITY JOURNAL; RAT; THALAMUS NUCLEUS;

ANIMALS; BRAIN DAMAGE, CHRONIC; CEREBELLUM; DISEASE MODELS, ANIMAL; EXCITATORY AMINO ACID ANTAGONISTS; GLUTAMIC ACID; HIPPOCAMPUS; HYPOXIA, BRAIN; INTRALAMINAR THALAMIC NUCLEI; MALE; MEMANTINE; MYOCLONUS; NERVE DEGENERATION; NEUROTOXINS; RATS; RATS, SPRAGUE-DAWLEY; RECEPTORS, N-METHYL-D-ASPARTATE; SYNAPTIC TRANSMISSION;

ANIMALIA; RATTUS;

EID: 33846285664     PISSN: 00068993     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.brainres.2006.11.076     Document Type: Article

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