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Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid

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Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid. / Baronio, Diego; Castro, Kamila; Gonchoroski, Taylor et al.

In: PLoS ONE, Vol. 10, No. 1, e0116363, 05.01.2015.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Baronio, D, Castro, K, Gonchoroski, T, de Melo, GM, Nunes, GDF, Bambini-Junior, V, Gottfried, C & Riesgo, R 2015, 'Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid', PLoS ONE, vol. 10, no. 1, e0116363. https://doi.org/10.1371/journal.pone.0116363

APA

Baronio, D., Castro, K., Gonchoroski, T., de Melo, G. M., Nunes, G. D. F., Bambini-Junior, V., Gottfried, C., & Riesgo, R. (2015). Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid. PLoS ONE, 10(1), [e0116363]. https://doi.org/10.1371/journal.pone.0116363

Vancouver

Baronio D, Castro K, Gonchoroski T, de Melo GM, Nunes GDF, Bambini-Junior V et al. Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid. PLoS ONE. 2015 Jan 5;10(1):e0116363. doi: 10.1371/journal.pone.0116363

Author

Baronio, Diego ; Castro, Kamila ; Gonchoroski, Taylor et al. / Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid. In: PLoS ONE. 2015 ; Vol. 10, No. 1.

Bibtex

@article{0ee6fac02a4d4194bfb26900f632ccd7,
title = "Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid",
abstract = "Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders primarily characterized by impaired social interaction and communication, and by restricted repetitive behaviors and interests. Ligands of histamine receptor 3 (H3R) are considered potential therapeutic agents for the treatment of different brain disorders and cognitive impairments. Considering this, the aim of the present study is to evaluate the actions of ciproxifan (CPX), an H3R antagonist, on the animal model of autism induced by prenatal exposure to valproic acid (VPA). Swiss mice were prenatally exposed to VPA on embryonic day 11 and assessed for social behavior, nociceptive threshold and repetitive behavior at 50 days of life. The treatment with CPX (3 mg/kg) or saline was administered 30 minutes before each behavioral test. The VPA group presented lower sociability index compared to VPA animals that were treated with CPX. Compared to the Control group, VPA animals presented a significantly higher nociceptive threshold, and treatment with CPX was not able to modify this parameter. In the marble burying test, the number of marbles buried by VPA animals was consistent with markedly repetitive behavior. VPA animals that received CPX buried a reduced amount of marbles. In summary, we report that an acute dose of CPX is able to attenuate sociability deficits and stereotypies present in the VPA model of autism. Our findings have the potential to help the investigations of both the molecular underpinnings of ASD and of possible treatments to ameliorate the ASD symptomatology, although more research is still necessary to corroborate and expand this initial data. ",
keywords = "Animals, Autistic Disorder/drug therapy, Behavior, Animal/drug effects, Disease Models, Animal, Female, Histamine Antagonists/pharmacology, Imidazoles/pharmacology, Mice, Pregnancy, Prenatal Exposure Delayed Effects/chemically induced, Receptors, Histamine H3/chemistry, Valproic Acid/toxicity",
author = "Diego Baronio and Kamila Castro and Taylor Gonchoroski and {de Melo}, {Gabriela Mueller} and Nunes, {Gustavo Della Flora} and Victorio Bambini-Junior and Carmem Gottfried and Rudimar Riesgo",
year = "2015",
month = jan,
day = "5",
doi = "10.1371/journal.pone.0116363",
language = "English",
volume = "10",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "1",

}

RIS

TY - JOUR

T1 - Effects of an H3R antagonist on the animal model of autism induced by prenatal exposure to valproic acid

AU - Baronio, Diego

AU - Castro, Kamila

AU - Gonchoroski, Taylor

AU - de Melo, Gabriela Mueller

AU - Nunes, Gustavo Della Flora

AU - Bambini-Junior, Victorio

AU - Gottfried, Carmem

AU - Riesgo, Rudimar

PY - 2015/1/5

Y1 - 2015/1/5

N2 - Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders primarily characterized by impaired social interaction and communication, and by restricted repetitive behaviors and interests. Ligands of histamine receptor 3 (H3R) are considered potential therapeutic agents for the treatment of different brain disorders and cognitive impairments. Considering this, the aim of the present study is to evaluate the actions of ciproxifan (CPX), an H3R antagonist, on the animal model of autism induced by prenatal exposure to valproic acid (VPA). Swiss mice were prenatally exposed to VPA on embryonic day 11 and assessed for social behavior, nociceptive threshold and repetitive behavior at 50 days of life. The treatment with CPX (3 mg/kg) or saline was administered 30 minutes before each behavioral test. The VPA group presented lower sociability index compared to VPA animals that were treated with CPX. Compared to the Control group, VPA animals presented a significantly higher nociceptive threshold, and treatment with CPX was not able to modify this parameter. In the marble burying test, the number of marbles buried by VPA animals was consistent with markedly repetitive behavior. VPA animals that received CPX buried a reduced amount of marbles. In summary, we report that an acute dose of CPX is able to attenuate sociability deficits and stereotypies present in the VPA model of autism. Our findings have the potential to help the investigations of both the molecular underpinnings of ASD and of possible treatments to ameliorate the ASD symptomatology, although more research is still necessary to corroborate and expand this initial data.

AB - Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders primarily characterized by impaired social interaction and communication, and by restricted repetitive behaviors and interests. Ligands of histamine receptor 3 (H3R) are considered potential therapeutic agents for the treatment of different brain disorders and cognitive impairments. Considering this, the aim of the present study is to evaluate the actions of ciproxifan (CPX), an H3R antagonist, on the animal model of autism induced by prenatal exposure to valproic acid (VPA). Swiss mice were prenatally exposed to VPA on embryonic day 11 and assessed for social behavior, nociceptive threshold and repetitive behavior at 50 days of life. The treatment with CPX (3 mg/kg) or saline was administered 30 minutes before each behavioral test. The VPA group presented lower sociability index compared to VPA animals that were treated with CPX. Compared to the Control group, VPA animals presented a significantly higher nociceptive threshold, and treatment with CPX was not able to modify this parameter. In the marble burying test, the number of marbles buried by VPA animals was consistent with markedly repetitive behavior. VPA animals that received CPX buried a reduced amount of marbles. In summary, we report that an acute dose of CPX is able to attenuate sociability deficits and stereotypies present in the VPA model of autism. Our findings have the potential to help the investigations of both the molecular underpinnings of ASD and of possible treatments to ameliorate the ASD symptomatology, although more research is still necessary to corroborate and expand this initial data.

KW - Animals

KW - Autistic Disorder/drug therapy

KW - Behavior, Animal/drug effects

KW - Disease Models, Animal

KW - Female

KW - Histamine Antagonists/pharmacology

KW - Imidazoles/pharmacology

KW - Mice

KW - Pregnancy

KW - Prenatal Exposure Delayed Effects/chemically induced

KW - Receptors, Histamine H3/chemistry

KW - Valproic Acid/toxicity

U2 - 10.1371/journal.pone.0116363

DO - 10.1371/journal.pone.0116363

M3 - Journal article

C2 - 25560049

VL - 10

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 1

M1 - e0116363

ER -