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Deletion of GAD67 in dopamine receptor‐1 expressing cells causes specific motor deficits
Author(s) -
Heusner Carrie L.,
Beutler Lisa R.,
Houser Carolyn R.,
Palmiter Richard D.
Publication year - 2008
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20405
Subject(s) - medium spiny neuron , dopamine , striatum , biology , glutamate decarboxylase , neuroscience , neurotransmitter , receptor , gabaergic , dopamine receptor d1 , direct pathway of movement , dopamine receptor d2 , enzyme , genetics , biochemistry
The medium spiny neurons (MSNs), which comprise the direct and indirect output pathways from the striatum, use γ‐aminobutyric acid (GABA) as their major fact‐acting neurotransmitter. We generated mice carrying a conditional allele of the Gad1 gene, which encodes GAD67, one of the two enzymes responsible for GABA biosynthesis, and bred them to mice expressing Cre recombinase at the dopamine D1 receptor locus ( Drd1a ) to selectively reduce GABA synthesis in the direct output pathway from the striatum. We show that these mice are deficient in some types of motor skills, but normal for others, suggesting a differential role for GABA release from D1 receptor‐containing neurons. genesis 46:357–367, 2008. © 2008 Wiley‐Liss, Inc.