Postnatal development of a GABA deficit and disturbance of neural functions in mice lacking GAD65-Reference-Cited by-同舟云学术

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Postnatal development of a GABA deficit and disturbance of neural functions in mice lacking GAD65

Published:2000-05 Issue:1 Volume:865 Page:45-58
ISSN:0006-8993
Container-title:Brain Research
language:en
Short-container-title:Brain Research

Author:

Stork Oliver,Ji Feng-Yun,Kaneko Koichi,Stork Simone,Yoshinobu Yuko,Moriya Takahiro,Shibata Shigenobu,Obata Kunihiko

Publisher

Elsevier BV

Subject

Developmental Biology,Clinical Neurology,Molecular Biology,General Neuroscience

Reference64 articles.

1. Inhibition of light- or glutamate-induced mPer1 expression represses the phase shifts into the mouse circadian locomotor and suprachiasmatic firing rhythms;Akiyama;J. Neurosci.,1999

2. Mice lacking the 65 kDa isoform of glutamic acid decarboxylase (GAD65) maintain normal levels of GAD67 and GABA in their brains but are susceptible to seizures;Asada;Biochem. Biophys. Res. Commun.,1996

3. Cleft palate and decreased brain gamma-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase;Asada;Proc. Natl. Acad. Sci. USA,1997

4. Effect of injection of antisense oligodeoxynucleotides of GAD isozymes into rat ventromedial hypothalamus on food intake and locomotor activity;Bannai;Brain Res.,1998

5. GABA-induced chemokinesis and NGF-induced chemotaxis of embryonic spinal cord neurons;Behar;J. Neurosci.,1994

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