GABA(A) receptor activation attenuates excitotoxicity but exacerbates oxygen-glucose deprivation-induced neuronal injury in vitro

Journal of Cerebral Blood Flow and Metabolism

Volumn 16, Issue 6, 1996, Pages 1211-1218

  Muir, Judith K ^a   Lobner, Doug ^a   Monyer, Hannelore ^b   Choi, Dennis W ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF HEIDELBERG   (Germany)

Author keywords

Baclofen; Glutamate; Ischemia; Muscimol; Neurotoxicity

Indexed keywords

4 AMINOBUTYRIC ACID RECEPTOR; BACLOFEN; CHLORIDE CHANNEL; GLUTAMIC ACID; MUSCIMOL; 4 AMINOBUTYRIC ACID A RECEPTOR; 4 AMINOBUTYRIC ACID B RECEPTOR; 4 AMINOBUTYRIC ACID RECEPTOR STIMULATING AGENT; GLUCOSE; OXYGEN;

ANIMAL CELL; ARTICLE; BRAIN PROTECTION; CALCIUM CELL LEVEL; CELL DEATH; CELL MEMBRANE STEADY POTENTIAL; GLUCOSE METABOLISM; IN VITRO STUDY; MEMBRANE POTENTIAL; MOUSE; NERVE INJURY; NEUROTRANSMITTER RELEASE; NONHUMAN; PRESYNAPTIC INHIBITION; PRIORITY JOURNAL; ANIMAL; BRAIN; CELL CULTURE; DRUG EFFECT; METABOLISM; NERVE CELL; PATHOLOGY;

ANIMALS; BACLOFEN; BRAIN; CELL DEATH; CELLS, CULTURED; GABA AGONISTS; GLUCOSE; MICE; MUSCIMOL; NEURONS; OXYGEN; RECEPTORS, GABA-A; RECEPTORS, GABA-B;

EID: 0029661967     PISSN: 0271678X     EISSN: None     Source Type: Journal    
DOI: 10.1097/00004647-199611000-00015     Document Type: Article

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