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Updated: Jul 9, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Developmental exposure to polychlorinated biphenyls PCB153 or PCB126 impairs learning ability in young but not in
Blanca Piedrafita1, Slaven Erceg, Omar Cauli
1Laboratory of Neurobiology, Centro de Investigacion Príncipe Felipe, Avda Autopista del Saler 16, 46013 Valencia, Spain.
Insights
Perinatal exposure to polychlorinated biphenyls (PCBs) impairs learning and brain pathway function in young rats, an effect absent in adults. This developmental neurotoxicity may explain cognitive deficits in children exposed to PCBs.
Area of Science:
- Environmental toxicology
- Neuroscience
- Developmental biology
Background:
- Polychlorinated biphenyls (PCBs) are persistent organic pollutants found in the food chain, human tissues, and milk.
- Prenatal and lactational PCB exposure is linked to cognitive impairment in children, but mechanisms are unclear.
- Some PCBs act as endocrine disruptors, potentially affecting neurodevelopment.
Purpose of the Study:
- To investigate the effects of perinatal exposure to PCB126 (dioxin-like) and PCB153 (non-dioxin-like) on learning and brain function in rats.
- To assess whether these effects differ between young (3 months) and adult (7-8 months) rats.
- To examine the involvement of the glutamate-nitric oxide (NO)-cGMP pathway in PCB-induced neurotoxicity.
Main Methods:
- Rats were exposed to PCB126 or PCB153 during pregnancy and lactation.
- Offspring were tested on a Y-maze conditional discrimination task at young and adult ages.
- In vivo brain microdialysis was used to analyze the glutamate-NO-cGMP pathway function in the cerebellum.
Main Results:
- Perinatal PCB exposure impaired learning and glutamate-NO-cGMP pathway function in young rats, but not in adults.
- PCB126 was significantly more potent than PCB153.
- Age-related declines in learning and pathway function observed in control rats were absent in PCB-exposed rats.
- Effects were similar in male and female rats.
Conclusions:
- Developmental exposure to PCBs impairs learning and the glutamate-NO-cGMP pathway in a manner dependent on age at testing.
- The glutamate-NO-cGMP pathway dysfunction induced during development may underlie PCB-associated cognitive deficits.
- PCB exposure disrupts normal age-related changes in cognitive function and neurochemistry.
Abstract:
Polychlorinated biphenyls (PCBs) are persistent organic pollutants present in the food chain and in human blood and milk. Exposure to PCBs during pregnancy and lactation leads to cognitive impairment in children. The underlying mechanisms remain unclear. Some PCBs are endocrine disrupters. The aim of this work was to assess whether exposure of rats to PCB126 (dioxin-like) or PCB153 (non-dioxin-like) during pregnancy and lactation affects the ability of the pups to learn a Y maze conditional discrimination task and/or the function of the glutamate-nitric oxide (NO)-cGMP pathway in brain in vivo when the rats are young (3 months) or adult (7-8 months). After finishing the learning experiments, the function of the pathway was analysed in the same rats by in vivo brain microdialysis. The results obtained show that perinatal exposure to PCB153 or PCB126: (1) impairs learning ability in young but not in adult rats, (2) impairs the glutamate-NO-cGMP pathway function in cerebellum in vivo in young but not in adult rats and (3) affect these parameters in males and females similarly. PCB126 is around 10 000-fold more potent than PCB153. In control rats the function of the glutamate-NO-cGMP pathway and learning ability are lower in adult than in young rats. These age-related differences are not present in rats exposed to PCBs. The impairment of the glutamate-NO-cGMP pathway function induced at young age by developmental exposure to the PCBs could be one of the mechanisms contributing to the cognitive impairment found in children whose mothers ingested PCB-contaminated food during pregnancy and lactation.
