(R)-ketamine attenuates neurodevelopmental disease-related phenotypes in a mouse model of maternal immune activation
Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes...
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| Published in | European archives of psychiatry and clinical neuroscience Vol. 273; no. 7; pp. 1501 - 1512 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.10.2023
Springer Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0940-1334 1433-8491 1433-8491 |
| DOI | 10.1007/s00406-023-01629-3 |
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| Abstract | Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 µg/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1β, IL-6, and TGF-β1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC. |
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| AbstractList | Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 µg/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1β, IL-6, and TGF-β1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC. Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 µg/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1β, IL-6, and TGF-β1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC.Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 µg/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1β, IL-6, and TGF-β1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC. Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 [micro]g/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1[beta], IL-6, and TGF-[beta]1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC. Infections during pregnancy are associated with an increased risk of neuropsychiatric disorders with developmental etiologies, such as schizophrenia and autism spectrum disorders (ASD). Studies have shown that the animal model of maternal immune activation (MIA) reproduces a wide range of phenotypes relevant to the study of neurodevelopmental disorders. Emerging evidence shows that (R)-ketamine attenuates behavioral, cellular, and molecular changes observed in animal models of neuropsychiatric disorders. Here, we investigate whether (R)-ketamine administration during adolescence attenuates some of the phenotypes related to neurodevelopmental disorders in an animal model of MIA. For MIA, pregnant Swiss mice received intraperitoneally (i.p.) lipopolysaccharide (LPS; 100 µg/kg/day) or saline on gestational days 15 and 16. The two MIA-based groups of male offspring received (R)-ketamine (20 mg/kg/day; i.p.) or saline from postnatal day (PND) 36 to 50. At PND 62, the animals were examined for anxiety-like behavior and locomotor activity in the open-field test (OFT), as well as in the social interaction test (SIT). At PND 63, the prefrontal cortex (PFC) was collected for analysis of oxidative balance and gene expression of the cytokines IL-1β, IL-6, and TGF-β1. We show that (R)-ketamine abolishes anxiety-related behavior and social interaction deficits induced by MIA. Additionally, (R)-ketamine attenuated the increase in lipid peroxidation and the cytokines in the PFC of the offspring exposed to MIA. The present work suggests that (R)-ketamine administration may have a long-lasting attenuation in deficits in emotional behavior induced by MIA, and that these effects may be attributed to its antioxidant and anti-inflammatory activity in the PFC. |
| Audience | Academic |
| Author | Lagranha, Claudia Jacques dos Santos Junior, Osmar Henrique de Santana, Jonata Henrique de Lima, Diógenes Afonso da Silva Júnior, José Carlos Gomes, Dayane Aparecida Duarte, Filipe Silveira de Oliveira, Elifrances Galdino de Souza Barbosa, Mayara Victória Lira, Eduardo Carvalho de Andrade Silva, Severina Cassia |
| Author_xml | – sequence: 1 givenname: Elifrances Galdino orcidid: 0000-0003-3745-4762 surname: de Oliveira fullname: de Oliveira, Elifrances Galdino email: Elifrances.galdino@ufpe.br organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego, Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco – sequence: 2 givenname: Diógenes Afonso surname: de Lima fullname: de Lima, Diógenes Afonso organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego – sequence: 3 givenname: José Carlos surname: da Silva Júnior fullname: da Silva Júnior, José Carlos organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego – sequence: 4 givenname: Mayara Victória surname: de Souza Barbosa fullname: de Souza Barbosa, Mayara Victória organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego – sequence: 5 givenname: Severina Cassia surname: de Andrade Silva fullname: de Andrade Silva, Severina Cassia organization: Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco, Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, Federal University of Pernambuco – sequence: 6 givenname: Jonata Henrique surname: de Santana fullname: de Santana, Jonata Henrique organization: Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco, Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, Federal University of Pernambuco – sequence: 7 givenname: Osmar Henrique surname: dos Santos Junior fullname: dos Santos Junior, Osmar Henrique organization: Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco, Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, Federal University of Pernambuco – sequence: 8 givenname: Eduardo Carvalho surname: Lira fullname: Lira, Eduardo Carvalho organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego – sequence: 9 givenname: Claudia Jacques surname: Lagranha fullname: Lagranha, Claudia Jacques organization: Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco, Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, Federal University of Pernambuco – sequence: 10 givenname: Filipe Silveira surname: Duarte fullname: Duarte, Filipe Silveira organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego – sequence: 11 givenname: Dayane Aparecida surname: Gomes fullname: Gomes, Dayane Aparecida organization: Laboratory of Neuroendocrinology and Metabolism, Department of Physiology and Pharmacology, Bioscience Center, Federal University of Pernambuco, Av. Prof. Moraes Rego, Graduate Program of Neuropsychiatry and Behavioral Sciences, Federal University of Pernambuco |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37249625$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
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| Keywords | Emotional behavior Inflammation Maternal immune activation Prefrontal cortex Oxidative imbalance (R)-ketamine |
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| SubjectTerms | Analysis Animal models Anti-inflammatory agents Anxiety Autism Cytokines Emotional behavior Gene expression Genetic aspects Health aspects Immune response Inflammation Interleukin 6 Ketamine Lipid peroxidation Lipopolysaccharides Locomotor activity Medical research Medicine Medicine & Public Health Medicine, Experimental Mental disorders Missing in action Nervous system diseases Neurodevelopmental disorders Neurosciences Offspring Open-field behavior Original Paper Phenotype Phenotypes Prefrontal cortex Pregnant women Psychiatry Schizophrenia Social aspects Social behavior Social interaction Transforming growth factor-b1 |
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| Title | (R)-ketamine attenuates neurodevelopmental disease-related phenotypes in a mouse model of maternal immune activation |
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