Myo-inositol treatment prevents biochemical changes triggered by kainate-induced status epilepticus

Neuroscience Letters

Volumn 468, Issue 3, 2010, Pages 277-281

  Solomonia, Revaz ^a,b   Mikautadze, Ekaterine ^a   Nozadze, Maia ^b   Kuchiashvili, Nino ^b   Lepsveridze, Eka ^a   Kiguradze, Tamar ^b  

^a I Chavchavadze State University   (United States)

^b Tbilisi St Andrew the First Called Georgian University of Georgian Patriarchate   (Georgia)

Author keywords

Calcium calmodulin dependent protein kinase II; Epilepsy; Glutamate receptors; Kainic acid; Myo inositol

Indexed keywords

CALCIUM CALMODULIN DEPENDENT PROTEIN KINASE II; GLUTAMATE RECEPTOR 1; HEAT SHOCK PROTEIN 90; INOSITOL; KAINIC ACID;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTICONVULSANT ACTIVITY; ARTICLE; BRAIN LEVEL; CONTROLLED STUDY; DRUG MECHANISM; EPILEPTIC STATE; GENETIC SUSCEPTIBILITY; HIPPOCAMPUS; LONG TERM CARE; MALE; NEOCORTEX; NONHUMAN; PRIORITY JOURNAL; RAT; WISTAR RAT;

ANIMALS; CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASE TYPE 2; CONVULSANTS; HIPPOCAMPUS; HSP90 HEAT-SHOCK PROTEINS; INOSITOL; KAINIC ACID; MALE; NEOCORTEX; RATS; RATS, WISTAR; RECEPTORS, AMPA; STATUS EPILEPTICUS;

EID: 72249112176     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neulet.2009.11.012     Document Type: Article

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