Homozygous GAD65 and heterozygous GAD67 knock-out mice reveal normal retinal development and maintenance despite reduced amounts of GABA.
May
Christian Albrecht
CA
Department of Anatomy, Carl Gustav Carus Medical Faculty, Technical University Dresden, 01307, Dresden, Germany. Albrecht.May@mailbox.tu-dresden.de
Nakamura
Kouichi
K
Fujiyama
Fumino
F
Komatsu
Yukio
Y
Yanagawa
Yuchio
Y
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*
D049452:Green Fluorescent Proteins; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; C401141:glutamate decarboxylase 2