Glial cell line-derived neurotrophic factor (GDNF) is an endogenous protector in the mesolimbic system against excessive alcohol consumption and relapse

Addiction Biology

Volumn 20, Issue 4, 2015, Pages 626-642

  Barak, Segev ^a,b,c   Wang, Jun ^a,b   Ahmadiantehrani, Somayeh ^a,b   Hamida, Sami Ben ^a,b,d   Kells, Adrian P ^b   Forsayeth, John ^b   Bankiewicz, Krystof S ^b   Ron, Dorit ^a,b  

^a UNIVERSITY OF CALIFORNIA SAN FRANCISCO   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c TEL AVIV UNIVERSITY   (Israel)

^d INSTITUT DE BIOLOGIE MOLÉCULAIRE ET CELLULAIRE   (France)

Author keywords

Alcohol addiction; dopamine; GDNF; nucleus accumbens; relapse; ventral tegmental area

Indexed keywords

ALCOHOL; GLIAL CELL LINE DERIVED NEUROTROPHIC FACTOR; SHORT HAIRPIN RNA; GDNF PROTEIN, RAT;

ALCOHOL CONSUMPTION; ALCOHOLISM; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIDROMIC STIMULATION; ARTICLE; BEHAVIOR CHANGE; BRAIN REGION; CELL ASSAY; CELL FUNCTION; CELL LEVEL; CONTROLLED STUDY; DISEASE ACTIVITY; DISEASE ASSOCIATION; DISEASE MARKER; DOPAMINERGIC NERVE CELL; DOWN REGULATION; DRINKING BEHAVIOR; GENE; GENE FUNCTION; GENE IDENTIFICATION; GLIAL CELL LINE DERIVED NEUROTROPHIC FACTOR GENE; LIMBIC SYSTEM; MALE; MOLECULAR DYNAMICS; MOLECULAR PATHOLOGY; NONHUMAN; NUCLEUS ACCUMBENS; PRIORITY JOURNAL; PROTEIN DETERMINATION; PROTEIN FUNCTION; PROTEIN LOCALIZATION; RAT; RELAPSE; UPREGULATION; VENTRAL TEGMENTUM; ADAPTATION; ANIMAL; DEFICIENCY; DRUG SELF ADMINISTRATION; GENE SILENCING; INSTRUMENTAL CONDITIONING; LONG EVANS RAT; PATHOPHYSIOLOGY; PHYSIOLOGY; RECURRENT DISEASE;

ADAPTATION, PHYSIOLOGICAL; ALCOHOL DRINKING; ANIMALS; CONDITIONING, OPERANT; DOPAMINERGIC NEURONS; DOWN-REGULATION; GENE KNOCKDOWN TECHNIQUES; GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR; LIMBIC SYSTEM; MALE; NUCLEUS ACCUMBENS; RATS, LONG-EVANS; RECURRENCE; SELF ADMINISTRATION; UP-REGULATION; VENTRAL TEGMENTAL AREA;

EID: 84930799718     PISSN: 13556215     EISSN: 13691600     Source Type: Journal    
DOI: 10.1111/adb.12152     Document Type: Article

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