title: Homozygous GAD65 and heterozygous GAD67 knock-out mice reveal normal retinal development and maintenance despite reduced amounts of GABA.
authors.affiliation: Department of Anatomy, Carl Gustav Carus Medical Faculty, Technical University Dresden, 01307, Dresden, Germany. Albrecht.May@mailbox.tu-dresden.de
authors.forename: Christian Albrecht
authors.initials: CA
authors.lastname: May
authors.forename: Kouichi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Fumino
authors.initials: F
authors.lastname: Fujiyama
authors.forename: Yukio
authors.initials: Y
authors.lastname: Komatsu
authors.forename: Yuchio
authors.initials: Y
authors.lastname: Yanagawa
mesh_terms: D000818:Animals; D005968:Glutamate Decarboxylase / Q000172:deficiency* / Q000235:genetics*; D049452:Green Fluorescent Proteins / Q000378:metabolism; D006579:Heterozygote; D006720:Homozygote; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D012160:Retina / Q000166:cytology / Q000254:growth & development*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D049452:Green Fluorescent Proteins; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; C401141:glutamate decarboxylase 2