Impact of GAD65 and/or GAD67 deficiency on perinatal development in rats.
GABA
GAD65
GAD67
knockout rats
phenotypes
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
revised:
26
11
2021
received:
03
09
2021
accepted:
13
12
2021
entrez:
31
12
2021
pubmed:
1
1
2022
medline:
13
1
2022
Statut:
ppublish
Résumé
GABA is a major neurotransmitter in the mammalian central nervous system. Glutamate decarboxylase (GAD) synthesizes GABA from glutamate, and two isoforms of GAD, GAD65, and GAD67, are separately encoded by the Gad2 and Gad1 genes, respectively. The phenotypes differ in severity between GAD single isoform-deficient mice and rats. For example, GAD67 deficiency causes cleft palate and/or omphalocele in mice but not in rats. In this study, to further investigate the functional roles of GAD65 and/or GAD67 and to determine the contribution of these isoforms to GABA synthesis during development, we generated various kinds of GAD isoform(s)-deficient rats and characterized their phenotypes. The age of death was different among Gad mutant rat genotypes. In particular, all Gad1
Identifiants
pubmed: 34972242
doi: 10.1096/fj.202101389R
doi:
Substances chimiques
Glutamate Decarboxylase
EC 4.1.1.15
glutamate decarboxylase 1
EC 4.1.1.15
glutamate decarboxylase 2
EC 4.1.1.15
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22123Informations de copyright
© 2021 Federation of American Societies for Experimental Biology.
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