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

机译：抗精神病药能逆转自发性高血压大鼠的情境恐惧调节缺陷：精神分裂症情绪情境处理的潜在动物模型吗？

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摘要

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.
机译：精神分裂症，双相情感障碍和注意力缺陷/多动障碍（ADHD）在情绪处理中表现出异常。先前的研究表明，自发性高血压大鼠（SHR）是ADHD的推定动物模型，其情境恐惧条件（CFC）减轻。本研究的目的是表征SHR提出的CFC中的赤字。成年雄性血压正常的Wistar大鼠和SHR接受了CFC任务。反复接触该任务后，研究了动物对电击的敏感性和CFC性能。药理学表征包括评估先前在获取CFC时使用的以下药物的作用：戊四唑（抗焦虑药）和氯二氮杂卓（抗焦虑药）；哌醋甲酯和苯丙胺（用于多动症）；拉莫三嗪，卡马西平和丙戊酸（情绪稳定剂）；氟哌啶醇，齐拉西酮，利培酮，氨磺必利和氯氮平（镇痛药）；甲氧氯普胺和SCH 23390（无抗精神病药特性的多巴胺拮抗剂）；和氯胺酮（一种模拟心理疗法）。还证实了自相矛盾的睡眠剥夺（使精神病症状恶化）的影响和潜在抑制方案（精神分裂症的动物模型）的表现。没有观察到对震动的敏感性差异。重复承担CFC任务并没有改变SHR提出的CFC赤字。考虑到药物治疗，只有抗精神病药可以逆转这种缺陷。这种缺陷通过前精神分裂症的操纵而增强。最后，SHR还提出了潜在抑制的缺陷。这些发现表明，由SHR呈现的CFC缺乏可能是研究与精神分裂症相关的情绪情境处理异常的有用动物模型。

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