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Long-term consequences of developmental exposure to lead or polychlorinated biphenyls: Synaptic transmission and

M E Gilbert¹, S M Lasley

¹Neurotoxicology Division (MD 74B), National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA.

Environmental Toxicology and Pharmacology

|July 26, 2011

Insights

Early exposure to lead (Pb) and polychlorinated biphenyls (PCBs) impairs cognitive development by disrupting synaptic plasticity in the brain. These neurotoxic effects on hippocampal long-term potentiation (LTP) may explain persistent cognitive deficits.

Area of Science:

Neuroscience
Developmental Toxicology
Environmental Health

Background:

Developmental exposure to lead (Pb) and polychlorinated biphenyls (PCBs) is linked to cognitive deficits in children.
These neurotoxic effects persist long after exposure ceases and body burdens decrease.
Mechanisms underlying Pb and PCB neurotoxicity remain unclear.

Purpose of the Study:

Investigate the impact of perinatal Pb and PCB exposure on hippocampal synaptic transmission and long-term potentiation (LTP).
Explore how these environmental toxicants affect activity-dependent plasticity during neural development.
Postulate that disruptions in plasticity lead to aberrant brain connectivity and cognitive impairment.

Main Methods:

Examined effects of Pb and PCBs on hippocampal synaptic transmission in animals exposed during the perinatal period.
Focused on long-term potentiation (LTP) as a model for use-dependent synaptic plasticity.
Analyzed potential alterations in activity-dependent plasticity and brain organization.

Main Results:

Perinatal exposure to Pb and PCBs detrimentally affects hippocampal synaptic transmission and LTP.
These neurotoxicants perturb activity-dependent plasticity crucial for establishing neural connections.
Aberrant connectivity may result from developmental disruptions in synaptic plasticity.

Conclusions:

Pb and PCBs interfere with activity-dependent synaptic plasticity during critical developmental periods.
Perturbations in plasticity can lead to lasting changes in brain organization and function.
Impaired hippocampal LTP and cognitive deficits in adulthood may stem from these developmental neurotoxic effects.

Read full analysis

Abstract:

Exposure to lead (Pb) or polychlorinated biphenyls (PCBs) during early development has been associated with deficits in cognitive function in children (Pediatrics 87 (1991) 219; N. Engl. J. Med. 335 (1996) 783). These effects persist in the child long after exposure has ceased and body burdens have diminished. Despite intensive research, no consensus on the mechanisms of neurotoxicity of these chemicals has resulted. As the primary neurotoxic action of these agents is to impair cognitive ability, a number of laboratories have examined and reported on the detrimental the effects of Pb or PCBs on hippocampal synaptic transmission and long-term potentiation (LTP) in animals exposed during the perinatal period. Use-dependent synaptic plasticity, of which hippocampal LTP is the primary model system, is a fundamental property of neuronal function. In forebrain structures such as amygdala and hippocampus, LTP and related processes are purported to represent a physiological substrate for memory. During brain ontogeny, this type of plasticity guides the establishment and maintenance of synaptic connections in cortical structures based on sensory input. We postulate that the actions of PCBs and Pb in the developing nervous system perturb activity-dependent plasticity and promote organizational changes in brain. Aberrant connectivity derived from perturbations in activity-dependent plasticity during development may manifest as impaired LTP and cognitive ability in the adult organism.

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