Immune activation in lactating dams alters sucklings' brain cytokines and produces non-overlapping behavioral deficits in adult female and male offspring: A novel neurodevelopmental model of sex-specific psychopathology

Arad, Michal; Piontkewitz, Yael; Albelda, Noa; Shaashua, Lee; Weiner, Ina

doi:10.1016/j.bbi.2017.01.015

Cited by 28 publications

(12 citation statements)

References 149 publications

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“…MIA may lead straightforwardly to damage to the foetal brain during the early stages of neurodevelopment (82), but may also provide entry into a deviant trajectory of neural development which predisposes offspring to behavioral deficits depending on the intensity of the infection and when in gestation it occurs [early vs. late-and potentially as late as the lactation stage (88)]. MIA-associated abnormalities have been described, sometimes inconsistently, for multiple brain cell types, all of which are implicated across psychiatric disorders from postmortem data and genetic studies to a greater or lesser extent: Schwann cells (89), astrocytes and microglia (90,91), hippocampal GABAergic cells (92,93), dopaminergic neurons (94), and parvalbumin interneurons (95,96).…”

Section: Experimental Paradigms Of Maternal Infectionmentioning

confidence: 99%

Schizophrenia and Influenza at the Centenary of the 1918-1919 Spanish Influenza Pandemic: Mechanisms of Psychosis Risk

et al. 2020

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Associations between influenza infection and psychosis have been reported since the eighteenth century, with acute "psychoses of influenza" documented during multiple pandemics. In the late 20 th century, reports of a season-of-birth effect in schizophrenia were supported by large-scale ecological and sero-epidemiological studies suggesting that maternal influenza infection increases the risk of psychosis in offspring. We examine the evidence for the association between influenza infection and schizophrenia risk, before reviewing possible mechanisms via which this risk may be conferred. Maternal immune activation models implicate placental dysfunction, disruption of cytokine networks, and subsequent microglial activation as potentially important pathogenic processes. More recent neuroimmunological advances focusing on neuronal autoimmunity following infection provide the basis for a model of infection-induced psychosis, potentially implicating autoimmunity to schizophrenia-relevant protein targets including the Nmethyl-D-aspartate receptor. Finally, we outline areas for future research and relevant experimental approaches and consider whether the current evidence provides a basis for the rational development of strategies to prevent schizophrenia.

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Section: Experimental Paradigms Of Maternal Infectionmentioning

confidence: 99%

Schizophrenia and Influenza at the Centenary of the 1918-1919 Spanish Influenza Pandemic: Mechanisms of Psychosis Risk

et al. 2020

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“…This mild to moderate dose was chosen based on previous studies showing that this concentration of the TLR-3 agonist could induce behavioral and cognitive alterations in mice (24)(25)(26). Therefore, experimental groups were challenged with a single injection of either Poly I:C or sterile saline at PND 45.…”

Section: Tlr-3 Agonist Administrationmentioning

confidence: 99%

Acute neuroinflammation elicited by TLR-3 systemic activation combined with early life stress induces working memory impairments in male adolescent mice

Viola

Creutzberg

Zaparte

et al. 2019

Behavioural Brain Research

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“…In recent years, the importance of immune function and the role of glial cells during brain development have been paid particular interest since new roles have been described in the interaction between the endocrine and immune systems under physiological and pathological conditions (Bilbo, Smith, & Schwarz, ; Harry & Kraft, ). Using prenatal or perinatal immune activation (Arad, Piontkewitz, Albelda, Shaashua, & Weiner, ; Canetta et al, ; Depino, ; Schaafsma et al, ), new evidence indicates the role of immune molecules in brain development and behavioral outcomes. For instance, the role in brain development and the plasticity of major histocompatibility complex I (MHCI), which mediates both innate and adaptive immune response, has been extensively studied (for a review, see Elmer & McAllister, ) and supports the idea that MHCI participates in several processes during brain development as in neural cell differentiation, migration, synapse formation/refinement, and synaptic transmission.…”

Section: Introductionmentioning

confidence: 99%

Role of the innate immune system in the neuropathological consequences induced by adolescent binge drinking

Pascual

Montesinos

2017

J of Neuroscience Research

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Adolescence is a critical stage of brain maturation in which important plastic and dynamic processes take place in different brain regions, leading to development of the adult brain. Ethanol drinking in adolescence disrupts brain plasticity and causes structural and functional changes in immature brain areas (prefrontal cortex, limbic system) that result in cognitive and behavioral deficits. These changes, along with secretion of sexual and stress-related hormones in adolescence, may impact self-control, decision making, and risk-taking behaviors that contribute to anxiety and initiation of alcohol consumption. New data support the participation of the neuroimmune system in the effects of ethanol on the developing and adult brain. This article reviews the potential pathological bases that underlie the effects of alcohol on the adolescent brain, such as the contribution of genetic background, the perturbation of epigenetic programming, and the influence of the neuroimmune response. Special emphasis is given to the actions of ethanol in the innate immune receptor toll-like receptor 4 (TLR4), since recent studies have demonstrated that by activating the inflammatory TLR4/NFκB signaling response in glial cells, binge drinking of ethanol triggers the release of cytokines/chemokines and free radicals, which exacerbate the immune response that causes neuroinflammation/neural damage as well as short- and long-term neurophysiological, cognitive, and behavioral dysfunction. Finally, potential treatments that target the neuroimmune response to treat the neuropathological and behavioral consequences of adolescent alcohol abuse are discussed.

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Immune activation in lactating dams alters sucklings' brain cytokines and produces non-overlapping behavioral deficits in adult female and male offspring: A novel neurodevelopmental model of sex-specific psychopathology

Cited by 28 publications

References 149 publications

Schizophrenia and Influenza at the Centenary of the 1918-1919 Spanish Influenza Pandemic: Mechanisms of Psychosis Risk

Schizophrenia and Influenza at the Centenary of the 1918-1919 Spanish Influenza Pandemic: Mechanisms of Psychosis Risk

Acute neuroinflammation elicited by TLR-3 systemic activation combined with early life stress induces working memory impairments in male adolescent mice

Role of the innate immune system in the neuropathological consequences induced by adolescent binge drinking

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