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Titolo:
A neurobiological basis for substance abuse comorbidity in schizophrenia
Autore:
Chambers, RA; Krystal, JH; Self, DW;
Indirizzi:
Connecticut Mental Hlth Ctr, Abraham Ribicoff Res Facil, New Haven, CT 06508 USA Connecticut Mental Hlth Ctr New Haven CT USA 06508 ew Haven, CT 06508 USA W Haven Vet Adm Hosp, Ribicoff Res Facil, New Haven, CT USA W Haven Vet Adm Hosp New Haven CT USA icoff Res Facil, New Haven, CT USA Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA Yale Univ New Haven CT USA iv, Sch Med, Dept Psychiat, New Haven, CT USA
Titolo Testata:
BIOLOGICAL PSYCHIATRY
fascicolo: 2, volume: 50, anno: 2001,
pagine: 71 - 83
SICI:
0006-3223(20010715)50:2<71:ANBFSA>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
VENTRAL TEGMENTAL AREA; NUCLEUS-ACCUMBENS NEURONS; MEDIAL PREFRONTAL CORTEX; FREELY-MOVING RATS; COCAINE-SEEKING BEHAVIOR; RECORDED IN-VITRO; LATENT INHIBITION; HIPPOCAMPAL DAMAGE; DOPAMINERGIC MECHANISMS; DRUG-ABUSE;
Keywords:
schizophrenia; substance abuse; dependence; dual diagnosis; dopamine; nucleus accumbens; hippocampus;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
146
Recensione:
Indirizzi per estratti:
Indirizzo: Chambers, RA Connecticut Mental Hlth Ctr, Abraham Ribicoff Res Facil, 3rd Floor,Room 331,34 Pk St, New Haven, CT 06508 USA Connecticut Mental Hlth Ctr 3rd Floor,Room 331,34 Pk St New Haven CT USA 06508
Citazione:
R.A. Chambers et al., "A neurobiological basis for substance abuse comorbidity in schizophrenia", BIOL PSYCHI, 50(2), 2001, pp. 71-83

Abstract

It is commonly held that substance use comorbidity in schizophrenia represents self-medication, an attempt by patients to alleviate adverse positive and negative symptoms, cognitive impairment, or medication side effects. However, recent advances suggest that increased vulnerability to addictive behavior may reflect the impact of the neuropathology of schizophrenia on theneural circuitry mediating drug reward and reinforcement. We hypothesize that abnormalities in the hippocampal formation and frontal cortex facilitate the positive reinforcing effects of drug reward and reduce inhibitory control over drug-seeking behavior. In this model, disturbances in drug rewardare mediated, in part, by, dysregulated neural integration of dopamine andglutamate signaling in the nucleus accumbens resulting form frontal cortical and hippocampal dysfunction. Altered integration of these signals would produce neural and motivational changes similar to long-term substance abuse but without the necessity of prior drug exposure. Thus, schizophrenic patients may have a predilection for addictive behavior as a primary disease symptom in parallel to, and in many cases independent from, their other symptoms. (C) 2001 Society of Biological Psychiatry.

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Documento generato il 18/01/20 alle ore 13:04:10