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

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 th...

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Veröffentlicht in:Schizophrenia bulletin 2009-07, Vol.35 (4), p.748-759
Hauptverfasser: Calzavara, Mariana Bendlin, Medrano, Wladimir Agostini, Levin, Raquel, Kameda, Sonia Regina, Andersen, Monica Levy, Tufik, Sergio, Silva, Regina Helena, Frussa-Filho, Roberto, Abílio, Vanessa Costhek
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container_issue 4
container_start_page 748
container_title Schizophrenia bulletin
container_volume 35
creator Calzavara, Mariana Bendlin
Medrano, Wladimir Agostini
Levin, Raquel
Kameda, Sonia Regina
Andersen, Monica Levy
Tufik, Sergio
Silva, Regina Helena
Frussa-Filho, Roberto
Abílio, Vanessa Costhek
description 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.
doi_str_mv 10.1093/schbul/sbn006
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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. 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Vascular system ; Conditioning (Psychology) - drug effects ; Conditioning (Psychology) - physiology ; Disease Models, Animal ; Dopamine Antagonists - pharmacology ; Electroshock ; Emotions - drug effects ; Fear - drug effects ; Fear - physiology ; Freezing Reaction, Cataleptic - drug effects ; Inhibition (Psychology) ; Male ; Medical sciences ; Memory - drug effects ; Neuropharmacology ; Pain Threshold - drug effects ; Pharmacology. Drug treatments ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psycholeptics: tranquillizer, neuroleptic ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychopharmacology ; Psychoses ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Wistar ; Regular ; Schizophrenia ; Schizophrenia - diagnosis ; Schizophrenia - drug therapy ; Schizophrenic Psychology ; Sleep Deprivation ; Vocalization, Animal - drug effects</subject><ispartof>Schizophrenia bulletin, 2009-07, Vol.35 (4), p.748-759</ispartof><rights>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. 2009</rights><rights>2009 INIST-CNRS</rights><rights>The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. 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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.</description><subject>Adult and adolescent clinical studies</subject><subject>Amphetamine - pharmacology</subject><subject>Animals</subject><subject>Antipsychotic Agents - pharmacology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Behavior, Animal - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Conditioning (Psychology) - drug effects</subject><subject>Conditioning (Psychology) - physiology</subject><subject>Disease Models, Animal</subject><subject>Dopamine Antagonists - pharmacology</subject><subject>Electroshock</subject><subject>Emotions - drug effects</subject><subject>Fear - drug effects</subject><subject>Fear - physiology</subject><subject>Freezing Reaction, Cataleptic - drug effects</subject><subject>Inhibition (Psychology)</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Memory - drug effects</subject><subject>Neuropharmacology</subject><subject>Pain Threshold - drug effects</subject><subject>Pharmacology. 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Arterial hypotension</topic><topic>Behavior, Animal - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Conditioning (Psychology) - drug effects</topic><topic>Conditioning (Psychology) - physiology</topic><topic>Disease Models, Animal</topic><topic>Dopamine Antagonists - pharmacology</topic><topic>Electroshock</topic><topic>Emotions - drug effects</topic><topic>Fear - drug effects</topic><topic>Fear - physiology</topic><topic>Freezing Reaction, Cataleptic - drug effects</topic><topic>Inhibition (Psychology)</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Memory - drug effects</topic><topic>Neuropharmacology</topic><topic>Pain Threshold - drug effects</topic><topic>Pharmacology. 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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.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>18281713</pmid><doi>10.1093/schbul/sbn006</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult and adolescent clinical studies
Amphetamine - pharmacology
Animals
Antipsychotic Agents - pharmacology
Arterial hypertension. Arterial hypotension
Behavior, Animal - drug effects
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Conditioning (Psychology) - drug effects
Conditioning (Psychology) - physiology
Disease Models, Animal
Dopamine Antagonists - pharmacology
Electroshock
Emotions - drug effects
Fear - drug effects
Fear - physiology
Freezing Reaction, Cataleptic - drug effects
Inhibition (Psychology)
Male
Medical sciences
Memory - drug effects
Neuropharmacology
Pain Threshold - drug effects
Pharmacology. Drug treatments
Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer
Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)
Psycholeptics: tranquillizer, neuroleptic
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychopharmacology
Psychoses
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Rats, Wistar
Regular
Schizophrenia
Schizophrenia - diagnosis
Schizophrenia - drug therapy
Schizophrenic Psychology
Sleep Deprivation
Vocalization, Animal - drug effects
title Neuroleptic Drugs Revert the Contextual Fear Conditioning Deficit Presented by Spontaneously Hypertensive Rats: A Potential Animal Model of Emotional Context Processing in Schizophrenia?
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