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Schizophrenia Bulletin Advance Access published online on February 16, 2008
Schizophrenia Bulletin, doi:10.1093/schbul/sbn006
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Neuroleptic Drugs Revert the Contextual Fear Conditioning Deficit Presented by Spontaneously Hypertensive Rats: A Potential Animal Model of Emotional Context Processing in Schizophrenia?

Mariana Bendlin Calzavara2, Wladimir Agostini Medrano2, Raquel Levin2, Sonia Regina Kameda2, Monica Levy Andersen3, Sergio Tufik3, Regina Helena Silva4, Roberto Frussa-Filho2 and Vanessa Costhek Abílio1,2
2 Department of Pharmacology and
3 Departament of Psychobiology, Universidade Federal de São Paulo, São Paulo, Brazil
4 Department of Physiology, Universidade Federal do Rio Grande do Norte, Natal, Brazil

1 To whom correspondence should be addressed; Departamento de Farmacologia, Universidade Federal de São Paulo, Rua Botucatu, 862 Ed. Leal Prado, CEP 04023-062, São Paulo, Brazil; tel/fax: +55-11-5576-4502, e-mail: abilio.farm{at}epm.br.

Schizophrenia, bipolar disorder, and attention deficit/hyperactivity disorder (ADHD) present abnormalities in emotion processing. A previous study showed that the spontaneously hypertensive rats (SHR), a putative animal model of ADHD, present reduced contextual fear conditioning (CFC). The aim of the present study was to characterize the deficit in CFC presented by SHR. Adult male normotensive Wistar rats and SHR were submitted to the CFC task. Sensitivity of the animals to the shock and the CFC performance after repeated exposure to the task were investigated. Pharmacological characterization consisted in the evaluation of the effects of the following drugs administered previously to the acquisition of the CFC: pentylenetetrazole (anxiogenic) and chlordiazepoxide (anxiolytic); methylphenidate and amphetamine (used for ADHD); lamotrigine, carbamazepine, and valproic acid (mood stabilizers); haloperidol, ziprasidone, risperidone, amisulpride, and clozapine (neuroleptic drugs); metoclopramide and SCH 23390 (dopamine antagonists without antipsychotic properties); and ketamine (a psychotomimmetic). The effects of paradoxical sleep deprivation (that worsens psychotic symptoms) and the performance in a latent inhibition protocol (an animal model of schizophrenia) were also verified. No differences in the sensitivity to the shock were observed. The repeated exposure to the CFC task did not modify the deficit in CFC presented by SHR. Considering pharmacological treatments, only the neuroleptic drugs reversed this deficit. This deficit was potentiated by proschizophrenia manipulations. Finally, a deficit in latent inhibition was also presented by SHR. These findings suggest that the deficit in CFC presented by SHR could be a useful animal model to study abnormalities in emotional context processing related to schizophrenia.

Keywords: rats / psychiatric disorder / emotional memory / antipsychotics / amphetamine / mood stabilizers


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