Adult rats that had been exposed before birth and during nursing to a mixture of chemicals found in a wide range of consumer products have a smaller medial prefrontal cortex (mPFC) and perform worse on an attention-switching task than rats not exposed to the chemicals early in life. These findings, published in JNeurosci, demonstrate a long-term influence of endocrine-disrupting compounds on brain development.
Phthalates -- chemicals used in plastics belonging to the same class as Bisphenol A (BPA) -- can potentially interfere with hormones important for the developing brain. Although previous studies have identified associations between phthalate exposure and developmental disturbances, little is known about the neurobiology underlying these relationships.
Researchers fed pregnant rats a daily cookie laced with human level doses of a chemical mixture based on data obtained from pregnant women. Pregnant dams orally consumed an environmentally relevant mixture of phthalates at 0, 200, or 1000 μg/kg/day through pregnancy and for 10 days while lactating. As adults, offspring were tested in an attentional set-shifting task, which assesses cognitive flexibility.
Authors also found that, independent of sex, perinatal phthalate exposure at either dose resulted in a reduction in neuron number, synapse number, and size of the mPFC and a deficit in cognitive flexibility. Interestingly, the number of synapses was correlated with cognitive flexibility, such that rats with fewer synapses were less cognitively flexible than those with more synapses.
As the mPFC is crucial for high level cognitive functions and reduced cognitive flexibility is observed in developmental disorders such as autism, the research shows how early life phthalate exposure can affect the brain and behavior.
Prenatal plastic chemical exposure linked to decreased cognitive ability in rats
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