Deletion of GAD67 in dopamine receptor-1 expressing cells causes specific motor deficits

Genesis

Volumn 46, Issue 7, 2008, Pages 357-367

  Heusner, Carrie L ^a   Beutler, Lisa R ^b   Houser, Carolyn R ^c,d   Palmiter, Richard D ^a,b  

^a UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF WASHINGTON   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d VA GREATER LOS ANGELES HEALTHCARE SYSTEM   (United States)

Author keywords

Behavior; Cre lox recombination; Dopamine; GABA; Striatum

Indexed keywords

4 AMINOBUTYRIC ACID; CRE RECOMBINASE; DOPAMINE 1 RECEPTOR; DOPAMINE RECEPTOR; DOPAMINE RECEPTOR 1A; GLUTAMATE DECARBOXYLASE; GLUTAMATE DECARBOXYLASE 1; GLUTAMATE DECARBOXYLASE 67;

4 AMINOBUTYRIC ACID METABOLISM; 4 AMINOBUTYRIC ACID RELEASE; ANIMAL BEHAVIOR; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; CORPUS STRIATUM; GABAERGIC TRANSMISSION; GAIT; GENE DELETION; GRIP STRENGTH; HANGING; HOMOLOGOUS RECOMBINATION; LOCOMOTION; MOTOR NEURON DISEASE; MOTOR PERFORMANCE; MOUSE; NEUROTRANSMISSION; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; ROTAROD TEST;

ANIMALS; BENZAZEPINES; BLOTTING, SOUTHERN; BLOTTING, WESTERN; CORPUS STRIATUM; GAMMA-AMINOBUTYRIC ACID; GLUTAMATE DECARBOXYLASE; IMMUNOHISTOCHEMISTRY; MICE; MICE, TRANSGENIC; MOTOR ACTIVITY; RECEPTORS, DOPAMINE;

MUS;

EID: 50849123750     PISSN: 1526954X     EISSN: 1526968X     Source Type: Journal    
DOI: 10.1002/dvg.20405     Document Type: Article

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