The point mutation gamma 2F77I changes the potency and efficacy of benzodiazepine site ligands in different GABAA receptor subtypes.
Ramerstorfer
Joachim
J
Department of Biochemistry and Molecular Biology, Center for Brain Research, Medical University Vienna, Spitalgasse 4, 1090 Vienna, Austria.
Furtmüller
Roman
R
Vogel
Elisabeth
E
Huck
Sigismund
S
Sieghart
Werner
W
D000818:Animals; D001569:Benzodiazepines / Q000378:metabolism*; D001665:Binding Sites; D002712:Chlorides / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D054314:Drug Inverse Agonism; D005260:Female; D058785:GABA-A Receptor Agonists; D006801:Humans; D008024:Ligands; D051379:Mice; D017354:Point Mutation; D051381:Rats; D011963:Receptors, GABA-A / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002712:Chlorides; D058785:GABA-A Receptor Agonists; D008024:Ligands; D011963:Receptors, GABA-A; D001569:Benzodiazepines; D005680:gamma-Aminobutyric Acid