Induction of metabolic hypofunction and neurochemical deficits after chronic intermittent exposure to phencyclidine: Differential modulation by antipsychotic drugs

Neuropsychopharmacology

Volumn 28, Issue 2, 2003, Pages 265-275

  Cochran, Susan M ^a   Kennedy, Matthew ^a,d   McKerchar, Clare E ^a   Steward, Lucinda J ^a,e   Pratt, Judith A ^a,b   Morris, Brian J ^a,c  

^a UNIVERSITY OF GLASGOW   (United Kingdom)

^b UNIVERSITY OF STRATHCLYDE   (United Kingdom)

^c UNIVERSITY OF GLASGOW   (United Kingdom)

^d UNIVERSITY OF BIRMINGHAM   (United Kingdom)

^e F HOFFMANN LA ROCHE LTD   (Switzerland)

Author keywords

Glucose utilization; NMDA receptor antagonist; Parvalbumin; Prefrontalcortex; Schizophrenia; Thalamus

Indexed keywords

NEUROLEPTIC AGENT; PARVALBUMIN; PHENCYCLIDINE;

ANIMAL; ARTICLE; BIOSYNTHESIS; CHEMICALLY INDUCED DISORDER; DISEASE MODEL; DRUG EFFECT; ENERGY METABOLISM; GENE EXPRESSION REGULATION; LONG EVANS RAT; MALE; METABOLISM; PHYSIOLOGY; PREFRONTAL CORTEX; RAT; SCHIZOPHRENIA; THALAMUS;

ANIMALS; ANTIPSYCHOTIC AGENTS; DISEASE MODELS, ANIMAL; ENERGY METABOLISM; GENE EXPRESSION REGULATION; MALE; PARVALBUMINS; PHENCYCLIDINE; PREFRONTAL CORTEX; RATS; RATS, LONG-EVANS; SCHIZOPHRENIA; THALAMUS;

EID: 0037308979     PISSN: 0893133X     EISSN: 1740634X     Source Type: Journal    
DOI: 10.1038/sj.npp.1300031     Document Type: Article

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