Dataset Information

Developmental exposure to concentrated ambient particles and preference for immediate reward in mice.

ABSTRACT:

Background

Recent epidemiological studies indicate negative associations between a diverse group of air pollutants and cognitive functioning in children and adults, and aspects of attention deficit in children. Neuroinflammation and oxidative stress are two putative biological mechanisms by which air pollutants may adversely affect the brain.

Objectives

We sought to determine whether exposure to concentrated ambient particulate matter (CAPS) during the first 2 weeks of life, alone or again in adulthood, could alter responding for delayed reward, a critical component of human decision making. Greater preference for immediate reward has been implicated as a component of several psychiatric disorders, addiction, obesity, and attention deficit.

Methods

C57BL/6J mice were exposed to ultrafine particles (< 100 nm in aerodynamic diameter; CAPS) using the Harvard University Concentrated Ambient Particle System (HUCAPS) or filtered air in the postnatal period (days 4-7 and 10-13) with and without adult exposure over days 56-60. In adulthood, delay behavior was assessed using a fixed-ratio waiting-for-reward (FR wait) paradigm in which 25 responses (FR25) were required to initiate the waiting-for-reward component during which mice obtained "free" sucrose pellets with the stipulation that these "free" pellets were delivered at increasing delay intervals.

Results

Coupled with increased FR response rates, mice exposed to postnatal CAPS displayed increased FR resets that reinstated short delays, indicating a preference for shorter delays, despite the added response cost of the FR25. No associated changes in locomotor activity were observed.

Conclusions

Postnatal CAPS exposure produces an enhanced bias towards immediate rewards, a risk factor for several central nervous system (CNS) disorders. This enhancement does not appear to be the result of hyperactivity. The findings underscore the need for further evaluation of air pollution effects on the CNS and its potential contribution to CNS diseases and disorders.

SUBMITTER: Allen JL

PROVIDER: S-EPMC3553438 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature

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Publications

Developmental exposure to concentrated ambient particles and preference for immediate reward in mice.

Allen Joshua L JL Conrad Katherine K Oberdörster Günter G Johnston Carl J CJ Sleezer Brianna B Cory-Slechta Deborah A DA

Environmental health perspectives 20121011 1

<h4>Background</h4>Recent epidemiological studies indicate negative associations between a diverse group of air pollutants and cognitive functioning in children and adults, and aspects of attention deficit in children. Neuroinflammation and oxidative stress are two putative biological mechanisms by which air pollutants may adversely affect the brain.<h4>Objectives</h4>We sought to determine whether exposure to concentrated ambient particulate matter (CAPS) during the first 2 weeks of life, alone ...[more]

PMID: 23063827

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Project description:BackgroundRecent epidemiological studies indicate early-life exposure to pollution particulate is associated with adverse neurodevelopmental outcomes. The need is arising to evaluate the risks conferred by individual components and sources of air pollution to provide a framework for the regulation of the most relevant components for public health protection. Previous studies in rodent models have shown diesel particulate matter has neurotoxic potential and could be a health concern for neurodevelopment. The present study shows an evaluation of pathological and protracted behavioral alterations following neonatal exposure to aerosolized diesel exhaust particles (NIST SRM 1650b). The particular behavioral focus was on temporal control learning, a broad and fundamental cognitive domain in which reward delivery is contingent on a fixed interval schedule. For this purpose, C57BL/6?J mice were exposed to aerosolized NIST SRM 1650b, a well-characterized diesel particulate material, from postnatal days 4-7 and 10-13, for four hours per day. Pathological features, including glial fibrillary-acidic protein, myelin basic protein expression in the corpus callosum, and ventriculomegaly, as well as learning alterations were measured to determine the extent to which NIST SRM 1650b would induce developmental neurotoxicity.ResultsTwenty-four hours following exposure significant increases in glial-fibrillary acidic protein (GFAP) in the corpus callosum and cortex of exposed male mice were present. Additionally, the body weights of juvenile and early adult diesel particle exposed males were lower than controls, although the difference was not statistically significant. No treatment-related differences in males or females on overall locomotor activity or temporal learning during adulthood were observed in response to diesel particulate exposure.ConclusionWhile some sex and regional-specific pathological alterations in GFAP immunoreactivity suggestive of an inflammatory reaction to SRM 1650b were observed, the lack of protracted behavioral and pathological deficits suggests further clarity is needed on the developmental effects of diesel emissions prior to enacting regulatory guidelines.

Project description:Ambient fine particulate matter (PM2.5) exposures during pregnancy could lead to adverse birth outcomes, including neurobehavioral development defects. However, limited studies explored the effects and potential epigenetic mechanisms of maternal PM2.5 exposure on offspring spatial memory defects. This study aims to explore the effects and underlying epigenetic mechanisms of maternal concentrated ambient PM2.5 exposure in male mice offspring with spatial memory defects. Pregnant female C57BL/6 mice were exposed daily to concentrated ambient PM2.5 (CAP) or filtered air (FA) throughout gestation, with the concentration of particulates (102.99 ± 78.74 μg/m3) and (2.78 ± 1.19 μg/m3), respectively. Adult male mice offspring were subsequently assessed for spatial learning and memory ability using Morris Water Maze tests and locomotor activities in open field tests. The hippocampus of the male mice offspring was harvested to test mRNA expression and DNA methylation. Results from the probe test of Morris Water Maze showed that the mice offspring in the CAP group had shorter swimming distance travelled in the target quadrant, shorter duration in the target quadrant, and less number of entries into the target quadrant (p < 0.05), suggesting spatial memory impairments. The acquisition trials of Morris Water Maze did not show a significant difference in learning ability between the groups. The mRNA level of interleukin 6 (IL-6) in the CAP group hippocampus (10.80 ± 7.03) increased significantly compared to the FA group (1.08 ± 0.43). Interestingly, the methylation levels of the CpG sites in the IL-6 promoter region declined significantly in the CAP group, (5.66 ± 0.83)% vs. (4.79 ± 0.48)%. Prenatal exposure to concentrated ambient PM2.5 induced long-lasting spatial memory defects in male mice offspring. The underlying biological mechanism might be mediated by an inflammatory reaction which is regulated by DNA methylation.

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Dataset Information

Developmental exposure to concentrated ambient particles and preference for immediate reward in mice.

Background

Objectives

Methods

Results

Conclusions

Publications

Developmental exposure to concentrated ambient particles and preference for immediate reward in mice.

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