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Titolo:
ASSESSING THE VALIDITY OF AN ANIMAL-MODEL OF DEFICIENT SENSORIMOTOR GATING IN SCHIZOPHRENIC-PATIENTS
Autore:
SWERDLOW NR; BRAFF DL; TAAID N; GEYER MA;
Indirizzi:
UNIV CALIF SAN DIEGO,SCH MED,DEPT PSYCHIAT,9500 GILMAN DR LA JOLLA CA92093
Titolo Testata:
Archives of general psychiatry
fascicolo: 2, volume: 51, anno: 1994,
pagine: 139 - 154
SICI:
0003-990X(1994)51:2<139:ATVOAA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSITRON EMISSION TOMOGRAPHY; ACOUSTIC STARTLE REFLEX; D2 DOPAMINE-RECEPTORS; PREPULSE INHIBITION; NUCLEUS-ACCUMBENS; ACTIVATING PROPERTIES; MESOLIMBIC DOPAMINE; RAT; ABNORMALITIES; STIMULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Social Sciences Citation Index
Science Citation Index Expanded
Citazioni:
84
Recensione:
Indirizzi per estratti:
Citazione:
N.R. Swerdlow et al., "ASSESSING THE VALIDITY OF AN ANIMAL-MODEL OF DEFICIENT SENSORIMOTOR GATING IN SCHIZOPHRENIC-PATIENTS", Archives of general psychiatry, 51(2), 1994, pp. 139-154

Abstract

Psychiatric researchers need specific animal models to better understand the neurobiology of schizophrenia. Prepulse inhibition (PPI), the reduction in startle produced by a prepulse stimulus, is diminished inschizophrenic patients. Theoretically, deficient PPI in schizophrenicpatients reflects a loss of sensorimotor gating that may lead to sensory flooding and cognitive fragmentation. In rats, PPI is disrupted bysystemic administration of dopamine agonists or by manipulations of neural circuitry linking the limbic cortex, striatum, pallidum, and pontine reticular formation. This loss of PPI in rats may be a useful model for studying the neurobiology of impaired sensorimotor gating in schizophrenic patients. We assessed the face, predictive, and construct validity of this animal model. Face validity was supported: stimulus manipulations produced parallel changes in PPI in humans and rats, and the dopamine agonist apomorphine disrupted PPI in rats, mimicking PPI deficits in schizophrenics. Predictive validity was supported: the ability of antipsychotics to restore PPI in apomorphine-treated rats correlated with clinical antipsychotic potency (r(s)=.991) and D-2-receptor affinity (r(s)=.893). Antipsychotics that restore PPI in apomorphine-treated rats include ''typical'' antipsychotics and the ''atypical'' antipsychotic clozapine. Construct validity was supported: PPI was disrupted in rats when dopamine was infused into the nucleus accumbens; this effect was blocked by haloperidol. The loss of PPI in dopamine-activated rats maybe a valid animal model of sensorimotor gating deficitsin schizophrenic patients. This model may help us understand the neurobiology of cognitive deficits in schizophrenic patients.

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Documento generato il 25/01/20 alle ore 16:28:56