Alcohol exposure during the developmental period induces α-endorphin neuronal death and causes alteration in the opioid control of stress axis function

Endocrinology

Volumn 148, Issue 6, 2007, Pages 2828-2834

  Sarkar, Dipak K ^a   Kuhn, Peter ^a   Marano, Jasson ^a   Chen, Cuiping ^a   Boyadjieva, Nadka ^a  

^a RUTGERS UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENYLATE CYCLASE; ALCOHOL; BETA ENDORPHIN; CORTICOTROPIN RELEASING FACTOR; CYCLIC AMP; LIPOPOLYSACCHARIDE; MESSENGER RNA; OPIATE; PROOPIOMELANOCORTIN; TRANSFORMING GROWTH FACTOR BETA1;

ALCOHOL CONSUMPTION; ANIMAL EXPERIMENT; APOPTOSIS; ARCUATE NUCLEUS; ARTICLE; CELL ACTIVITY; CONTROLLED STUDY; DEVELOPMENTAL STAGE; FEMALE; HYPOTHALAMUS; IN VIVO STUDY; LASER CAPTURE MICRODISSECTION; NERVE CELL NECROSIS; NERVE ENDING; NEWBORN; NONHUMAN; NUCLEOTIDE SEQUENCE; PERIKARYON; PREGNANCY; PRIORITY JOURNAL; RAT; STRESS; THALAMUS MIDLINE NUCLEUS;

ANIMALS; ANIMALS, NEWBORN; APOPTOSIS; APOPTOSIS REGULATORY PROTEINS; BETA-ENDORPHIN; CELL DEATH; CORTICOTROPIN-RELEASING HORMONE; CYCLIC AMP; ETHANOL; FEMALE; HYPOTHALAMUS; NEURONS; PRESYNAPTIC TERMINALS; RATS; RATS, SPRAGUE-DAWLEY; STRESS; TRANSFORMING GROWTH FACTOR BETA1;

EID: 34250904380     PISSN: 00137227     EISSN: 00137227     Source Type: Journal    
DOI: 10.1210/en.2006-1606     Document Type: Article

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