Animal models of autism with a particular focus on the neural basis of changes in social behaviour: An update article

Olexová, Lucia; Talarovičová, Alžbeta; Lewis-Evans, Ben; Borbélyová, Veronika; Kršková, Lucia

doi:10.1016/j.neures.2012.10.004

Cited by 11 publications

(10 citation statements)

References 160 publications

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“…A number of animal models have been created in autism research that imitates changes observed in the autistic population, especially social deficit (Olexová et al, 2012). One animal model of autism is rats that have been treated prenatally with valproic acid -VPA rats (Rodier et al, 1996(Rodier et al, , 1997Schneider and Przewlocki, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the impairment of social behaviour seen in autistic individuals could be the result of atypical development in these regions (Pelphrey and Carter, 2008). In addition to the areas comprising the "social brain", alteration in other brain structures (Olexová et al, 2012) including the hypothalamus -the structure responsible for the synthesis and secretion of the OT and AVP neuropeptides have also been recognized as being involved in the social deficit observed in autistic populations (Kurth et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Increased sociability and gene expression of oxytocin and its receptor in the brains of rats affected prenatally by valproic acid

Štefánik

Olexová

Kršková

2015

Pharmacology Biochemistry and Behavior

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased sociability and gene expression of oxytocin and its receptor in the brains of rats affected prenatally by valproic acid

Štefánik

Olexová

Kršková

2015

Pharmacology Biochemistry and Behavior

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“…Animal models show varying amounts of resemblance to autism ranging from genetic models with specific mutations to broad interventions such as perinatal valproic acid treatment. Borna disease virus infection, VPA rats and BTBR T/+ mouse were suggested as the models which show differences in most brain structures that are similar to those seen in autistic individuals as well as showing behavioural patterns similar to social deficit [49].…”

Section: Discussionmentioning

confidence: 99%

“…On macaques, bilateral lesions of the amygdala resulted in less social contacts and showed more social withdrawal than control subjects [46]. While ablation of superior temporal sulcus region reveal difficulties in responding to social cues like eye gaze [48], Olexová et al [49] have stated that more extensive lesions of the medial temporal lobe, including the amygdala, hippocampus and ventromedial temporal cortex initiated an even more profound effect on the social interactions of macaques, including a 'lack of social skills' and flat affect [49].…”

Section: Animal Models Obtained By Destruction Of Certain Cns Areasmentioning

confidence: 99%

Animal Models of Autism Spectrum Disorder

Erdoğan¹

2017

JNSK

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Animal models are developed to test hypotheses about causes of disease, and potential treatments. With genetic, molecular, imaging and electrophysiological studies being supported by animal models, autism research has been flourishing in recent years. On different aspects of autism research, a significant number of reviews have been published. Several of them treated animal models to help current knowledge around its etiology while some others had standpoint of species or neuroanatomical findings. In this article, we present an overview of the animal models.Keywords: Autism spectrum disorder; Animal models most widely used animal in neuroscience [1]. Mouse models have also been used often by the neuroscience community. As compared to mice, rats promise more advantages; with richer social behavioural repertoire, they show various types of social behaviours and use a rich communication system [2]. Surgical experiments, histopathological evaluation, electrophysiological recordings are easier in rats by reason of their larger size. Furthermore, they have the capability of being the major objects of pharmaceutical industry in testing drug efficacy, dosage and toxicology. However animal models on genetic alterations were defined in mice so far.Recently different animals like the zebrafish (Danio Rerio) has also become a popular model organism in neuroscience to study ASD. It seems to be a strong model organism due to representation of highly social animals and looks promising for complementing traditional rodent models [3]. Because of the capacity of vocal learning, songbird animal model was supposed to contribute important insights to our understanding of the communication deficits in ASD [4]. Besides social features, they display characteristically human traits like monogamy and cultural inheritance. Due to its high degree of correspondence to human behavior and their striking homology in the anatomy of neural circuits that mediate social behavior, non-human primate (NHP) model is largely believed to help bridge the gap between humans and lower vertebrate systems [5]. Use of NHP model has the advantages of contributing to some more behavioral aspects of ASD research. However, ethical implications of NHP research and the absence of genetic knockouts in NHP models tend to pose limitations [6]. Surprisingly, a fruit fly, Drosophila and a sea hare, Aplysia and a nematode, C. elegans provide the potential of carrying out large scale screens using the sophisticated genetic tools available despite being millions of years apart on the evolutionary scale. They are likely to facilitate the dissection of the genetic basis of ASD [6].According to a common hypothesis, ASD results from the interaction of a genetic predisposition and an early environmental insult [7]. We have chosen to focus on methodology in conducting the animal models for ASD. Therefore, we thought that it would be efficacious to reveal keypoints by following the mechanisms set up in animal models. Genetically Manipulated Animal ModelsNumerous candidate...

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“…Сам белок участвует в дифференциации аксонов на отдельные локальные части. Мыши, у которых отсут-ствовал этот белок, имели симптомы РАС, а также гиперактивность и эпилептические припадки [41]. Идентифицированы гены ARID1B, CHD8, DYRK1A, grin2b, SCN2A, которые тоже повышают риск раз-вития аутизма, но пока нет более точных данных об этих животных моделях.…”

Section: моделирование аутизма в экспериментах на животныхunclassified

Autism spectrum disorders: etiology, treatment. models and experimental studies

Lavrov

Васильевич²,

Shabanov

et al. 2018

Rev Clin Pharm Drug Ther

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Резюмее.Изучение расстройств мозговой деятель-ности при снижении социализации является актуаль-ной современной проблемой. В статье представлен обзор литературных данных относительно эпидемиологии, этиологии и лечения расстройств аутистического спек-тра. Особое внимание уделяется экспериментальным моделям аутизма, поскольку именно моделирование позволяет проверить гипотезы относительно природы заболевания и провести апробацию новых лечебных методов. AAbstrasе.The study of disorders of brain activity related to the violation of socialization is the current scientific problem. The article presents a review of the literature regarding the epidemiology, etiology and treatment of autism spectrum disorders. Special attention is paid to experimental models of autism, since simulation allows to test hypotheses about the nature of the disease and to carry out testing of new treatment methods. Keywtrb:autism spectrum disorders; epidemiology; etiology; pharmacotherapy; psychotherapy; experimental modeling. ВВеденИеВыяснение мозговых механизмов социальной дез адаптации составляет проблему, актуальность которой возрастает по мере прогресса общества и расширения масштабов межличностной комму-никации. Сниженная социализация у ребенка нега-тивно влияет на внутрисемейные взаимоотношения и угрожает семейной целостности [8]. Поскольку наиболее отчетливо дезадаптационные механиз-мы проявляются в условиях психоэмоциональной и орга нической патологии ЦНС, исследование меха-низмов основывается на клинических данных и моде-лях, воспроизводящих поведенческие расстройства.Патологию, определяемую как «аутизм» (от греч. αὐτός -сам), впервые подробно описал в 1911 г. швейцарский психиатр E. Bleuler [20]. Именно он предложил заменить диагноз dementia praecox (пре-ждевременное слабоумие) термином «шизофре-ния». При этом он объединял аутизм с шизофрени-ей и считал, что он выступает одним из частных ее проявлений. Благодаря накоплению знаний отно-сительно мозговой организации углублялось по-нимание природы аутизма. L. Kanner [35], один из основоположников детской психиатрии, классифи-цировал «детский аутизм» в качестве отдельного за-болевания и обозначил момент его возникновения. Было отмечено, что заболевание проявляется в воз-

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Animal models of autism with a particular focus on the neural basis of changes in social behaviour: An update article

Cited by 11 publications

References 160 publications

Increased sociability and gene expression of oxytocin and its receptor in the brains of rats affected prenatally by valproic acid

Increased sociability and gene expression of oxytocin and its receptor in the brains of rats affected prenatally by valproic acid

Animal Models of Autism Spectrum Disorder

Autism spectrum disorders: etiology, treatment. models and experimental studies

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