Effects of maternal immune activation on adult neurogenesis in the subventricular zone–olfactory bulb pathway and olfactory discrimination

Liu, Yuan Hsuan; Lai, Wen-Sung; Tsay, Huey Jen; Wang, Tsu Wei; Yu, Jenn Yah

doi:10.1016/j.schres.2013.09.007

Cited by 32 publications

(21 citation statements)

References 69 publications

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“…In principle, PC cerebellar hyperplasia might be due to either increased neurogenesis or reduced programmed cell death. However, because poly(I:C) was administered beyond the main window of PC birth (E10-E13 [40]) it is not evident how additional (heterochronic) PC neurogenesis might be stimulated, and in other brain regions, maternal immune activation results in reduced neurogenesis (e.g., hippocampus [15,72], olfactory bulb [73], cortex [74], etc.). Indeed, there appears to be no evidence that neurogenesis is stimulated by maternal immune activation anywhere in the brain.…”

Section: Discussionmentioning

confidence: 99%

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

et al. 2015

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There have been suggestions that maternal immune activation is associated with alterations in motor behavior in offspring. To explore this further, we treated pregnant mice with polyinosinic:polycytidylic acid (poly(I:C)), a viral mimetic that activates the innate immune system, or saline on embryonic days 13-15. At postnatal day (P) 18, offspring cerebella were collected from perfused brains and immunostained as whole-mounts for zebrin II. Measurements of zebrin II+/- stripes in both sexes indicated that prenatal poly(I:C)-exposed offspring had significantly wider stripes; this difference was also seen in similarly treated offspring in adulthood (~P120). When sagittal sections of the cerebellum were immunostained for calbindin and Purkinje cell numbers were counted, we observed greater numbers of Purkinje cells in poly(I:C) offspring at both P18 and ~ P120. In adolescence (~P40), both male and female prenatal poly(I:C)-exposed offspring exhibited poorer performance on the rotarod and ladder rung tests; deficits in performance on the latter test persisted into adulthood. Offspring of both sexes from poly(I:C) dams also exhibited impaired social interaction in adolescence, but this difference was no longer apparent in adulthood. Our results suggest that maternal immune exposure at a critical time of cerebellum development can enhance neuronal survival or impair normal programmed cell death of Purkinje cells, with lasting consequences on cerebellar morphology and a variety of motor and non-motor behaviors.

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Section: Discussionmentioning

confidence: 99%

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

et al. 2015

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“…The occurrence of such disruptions is dependent on the timing of early-life challenge and has been reported most often in mature animals (Meyer et al, 2006a(Meyer et al, , 2008b. Moreover, the consequences of reprogramming the brain following exposure to inflammatory mediators such as lipopolysaccharide (LPS) and polyriboinosinic-polyribocytidilic acid (Poly:IC) appear to have a regulated time course (Harre´et al, 2008;Forrest et al, 2012;Garay et al, 2013;Khalil et al, 2013;Liu et al, 2013). For example, neonatal (n)LPS led to hippocampal NMDA receptor subtype expression that was juxtaposed between acute (i.e., increased expression) and chronic (i.e., decreased expression) time points (Harre´et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Tracing the trajectory of behavioral impairments and oxidative stress in an animal model of neonatal inflammation

et al. 2015

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“…50 Defects in neurogenesis are associated with ASD both in humans 43 and in the MIA mouse model of ASD. 51 The brains of the mice exposed to/fed the high-GI diet from conception showed decreased levels of DCX, a protein marker of neurogenesis whose expression is uniquely associated with neuron-restricted progenitors and differentiating neurons, 52 relative to the brains of the mice exposed to/fed the low-GI diet from conception. DCX was previously shown to be lower in the brains of BTBR mice relative to control C57BL/6 mice, which do not show an ASD phenotype.…”

Section: Discussionmentioning

confidence: 99%

Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder

et al. 2015

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Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder of unknown etiology, but very likely resulting from both genetic and environmental factors. There is good evidence for immune system dysregulation in individuals with ASD. However, the contribution of insults such as dietary factors that can also activate the immune system have not been explored in the context of ASD. In this paper, we show that the dietary glycemic index has a significant impact on the ASD phenotype. By using BTBR mice, an inbred strain that displays behavioral traits that reflect the diagnostic symptoms of human ASD, we found that the diet modulates plasma metabolites, neuroinflammation and brain markers of neurogenesis in a manner that is highly reflective of ASD in humans. Overall, the manuscript supports the idea that ASD results from gene-environment interactions and that in the presence of a genetic predisposition to ASD, diet can make a large difference in the expression of the condition.

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Effects of maternal immune activation on adult neurogenesis in the subventricular zone–olfactory bulb pathway and olfactory discrimination

Cited by 32 publications

References 69 publications

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

Tracing the trajectory of behavioral impairments and oxidative stress in an animal model of neonatal inflammation

Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder

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