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Ontogenetic alterations in molecular and structural correlates of dendritic growth after developmental exposure to
Pamela J Lein1, Dongren Yang, Adam D Bachstetter
1Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, Portland, Oregon, USA.
Insights
Developmental exposure to polychlorinated biphenyls (PCBs) alters brain development, accelerating dendritic growth in key regions. This disruption in neuronal connectivity may explain cognitive deficits observed in children exposed to PCBs.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Perinatal polychlorinated biphenyl (PCB) exposure is linked to cognitive and behavioral deficits in children.
- These deficits are hypothesized to stem from altered neuronal connectivity.
Purpose of the Study:
- To investigate the impact of developmental PCB exposure on dendritic growth in the brain.
- To test the hypothesis that altered neuronal connectivity underlies PCB-induced neurodevelopmental effects.
Main Methods:
- Rat dams received Aroclor 1254 (a PCB mixture) or vehicle from gestation through postnatal day 21.
- Dendritic growth and gene expression (spinophilin, RC3/neurogranin) were analyzed in hippocampal and cerebellar neurons.
Main Results:
- Developmental PCB exposure led to an age-related increase in dendritic growth, with accelerated growth rates at later ages.
- While dendritic lengths were initially reduced, they became comparable to or exceeded controls by postnatal day 60.
- PCB exposure increased spinophilin and RC3/neurogranin mRNA expression in the brain, particularly in the cortex.
Conclusions:
- Developmental PCB exposure significantly alters the timing and extent of dendritic growth in critical brain regions.
- These changes in dendritogenesis support the hypothesis that disrupted neuronal connectivity contributes to the neuropsychological deficits associated with PCB exposure.
Objective:
Perinatal exposure to polychlorinated biphenyls (PCBs) is associated with decreased IQ scores, impaired learning and memory, psychomotor difficulties, and attentional deficits in children. It is postulated that these neuropsychological deficits reflect altered patterns of neuronal connectivity. To test this hypothesis, we examined the effects of developmental PCB exposure on dendritic growth.
Methods:
Rat dams were gavaged from gestational day 6 through postnatal day (PND) 21 with vehicle (corn oil) or the commercial PCB mixture Aroclor 1254 (6 mg/kg/day). Dendritic growth and molecular markers were examined in pups during development.
Results:
Golgi analyses of CA1 hippocampal pyramidal neurons and cerebellar Purkinje cells indicated that developmental exposure to PCBs caused a pronounced age-related increase in dendritic growth. Thus, even though dendritic lengths were significantly attenuated in PCB-treated animals at PND22, the rate of growth was accelerated at later ages such that by PND60, dendritic growth was comparable to or even exceeded that observed in vehicle controls. Quantitative reverse transcriptase polymerase chain reaction analyses demonstrated that from PND4 through PND21, PCBs generally increased expression of both spinophilin and RC3/neurogranin mRNA in the hippocampus, cerebellum, and cortex with the most significant increases observed in the cortex.
Conclusions:
This study demonstrates that developmental PCB exposure alters the ontogenetic profile of dendritogenesis in critical brain regions, supporting the hypothesis that disruption of neuronal connectivity contributes to neuropsychological deficits seen in exposed children.
